JoVE Visualize What is visualize?
Stop Reading. Start Watching.
Advanced Search
Stop Reading. Start Watching.
Regular Search
Find video protocols related to scientific articles indexed in Pubmed.
Genome-wide association study identifies three susceptibility loci for laryngeal squamous cell carcinoma in the Chinese population.
Nat. Genet.
PUBLISHED: 09-07-2014
Show Abstract
Hide Abstract
To identify genetic markers for laryngeal squamous cell carcinoma (LSCC), we conducted a genome-wide association study (GWAS) on 993 individuals with LSCC (cases) and 1,995 cancer-free controls from Chinese populations. The most promising variants (association P < 1 × 10(-5)) were then replicated in 3 independent sets including 2,398 cases and 2,804 controls, among which we identified 3 new susceptibility loci at 11q12 (rs174549), 6p21 (rs2857595) and 12q24 (rs10492336). The minor alleles of each of these loci showed protective effects, with odds ratios (95% confidence intervals) of 0.73 (0.68-0.78; P = 1.00 × 10(-20)), 0.78 (0.72-0.84; P = 2.43 × 10(-15)) and 0.71 (0.65-0.77; P = 4.48 × 10(-14)), respectively. None of these variants showed an interaction with smoking or drinking. This is the first GWAS to our knowledge solely on LSCC, and the findings might advance understanding of the etiology of LSCC.
Related JoVE Video
Emergency treatment of splenic injury in a novel mobile minimally invasive interventional shelter following disaster: a feasibility study.
Scand J Trauma Resusc Emerg Med
PUBLISHED: 08-09-2014
Show Abstract
Hide Abstract
There has been an increase in natural disasters in recent years, which leads to a great number of injuries and deaths. It still remains an unsolved problem to treat patients with vascular injury of solid organs effectively following natural disasters, but on-spot emergency interventional transcatheter arterial embolization (TAE) has been highly recommended to cure serious vascular injury of solid organs nowadays. Spleen is the most vulnerable abdominal organ, severe arterial hemorrhage of which can cause death if untreated timely. In this research, we aimed to study the possibility of performing emergency surgical intervention in mobile minimally invasive interventional shelter for splenic injury in the case of natural disasters.
Related JoVE Video
Hyperhomocysteinemia potentiates hyperglycemia-induced inflammatory monocyte differentiation and atherosclerosis.
Diabetes
PUBLISHED: 07-09-2014
Show Abstract
Hide Abstract
Hyperhomocysteinemia (HHcy) is associated with increased diabetic cardiovascular diseases. However, the role of HHcy in atherogenesis associated with hyperglycemia (HG) remains unknown. To examine the role and mechanisms by which HHcy accelerates HG-induced atherosclerosis, we established an atherosclerosis-susceptible HHcy and HG mouse model. HHcy was established in mice deficient in cystathionine ?-synthase (Cbs) in which the homocysteine (Hcy) level could be lowered by inducing transgenic human CBS (Tg-hCBS) using Zn supplementation. HG was induced by streptozotocin injection. Atherosclerosis was induced by crossing Tg-hCBS Cbs mice with apolipoprotein E-deficient (ApoE(-/-)) mice and feeding them a high-fat diet for 2 weeks. We demonstrated that HHcy and HG accelerated atherosclerosis and increased lesion monocytes (MCs) and macrophages (MØs) and further increased inflammatory MC and MØ levels in peripheral tissues. Furthermore, Hcy-lowering reversed circulating mononuclear cells, MC, and inflammatory MC and MC-derived MØ levels. In addition, inflammatory MC correlated positively with plasma Hcy levels and negatively with plasma s-adenosylmethionine-to-s-adenosylhomocysteine ratios. Finally, l-Hcy and d-glucose promoted inflammatory MC differentiation in primary mouse splenocytes, which was reversed by adenoviral DNA methyltransferase-1. HHcy and HG, individually and synergistically, accelerated atherosclerosis and inflammatory MC and MØ differentiation, at least in part, via DNA hypomethylation.
Related JoVE Video
Contribution of homeostatic chemokines CCL19 and CCL21 and their receptor CCR7 to coronary artery disease.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 07-02-2014
Show Abstract
Hide Abstract
Our aim was to identify the role of the homeostatic chemokines CCL19 and CCL21 and their common receptor CCR7 in atherogenesis and to study the relationships between CCL19, CCL21, and CCR7 gene variants and coronary artery disease in a Chinese Han population.
Related JoVE Video
Breast cancer metastasis to the stomach confirmed using gastroscopy: A case report.
Oncol Lett
PUBLISHED: 06-17-2014
Show Abstract
Hide Abstract
Breast cancer metastasis to the stomach is relatively rare. Unlike infiltrating ductal carcinoma, invasive lobular carcinoma (ILC) has a high tendency to metastasize to the stomach. The present study reports a case of a 53-year-old female who had undergone a modified radical mastectomy of the left breast for ILC eight years previously and presented at the clinic seeking treatment for epigastric discomfort from sour regurgitation and belching that had persisted for one month. Gastroscopy revealed multiple apophysis lesions in the stomach, which were diagnosed as metastatic tumors to the stomach. The diagnosis was further established using histological and immunohistochemical analyses for gross cystic disease fluid protein-15, cytokeratin (CK) 7 and CK20. The patient was treated with systemic chemotherapy without surgery. During the treatment, two gastroscopy procedures revealed that the apophysis lesions in the gastric body had narrowed significantly. Few cases of breast cancer metastasizing to the stomach have been reported, particularly those that have been confirmed using gastroscopy. The present study reports a case of breast cancer metastasis to the stomach to raise awareness of the condition.
Related JoVE Video
Age, estimated glomerular filtration rate and ejection fraction score predicts contrast-induced acute kidney injury in patients with diabetes and chronic kidney disease: insight from the TRACK-D study.
Chin. Med. J.
PUBLISHED: 06-17-2014
Show Abstract
Hide Abstract
The occurrence of contrast induced acute kidney injury (CIAKI) has a pronounced impact on morbidity and mortality. The aim of the present study was to appraise the diagnostic efficacy of age, estimated glomerular filtration rate (eGFR) and ejection fraction (AGEF) score (age/EF(%)+1 (if eGFR was <60 ml × min(-1)× 1.73 m(-2))) as an predictor of CIAKI in patients with diabetes mellitus (DM) and concomitant chronic kidney disease (CKD).
Related JoVE Video
CREG promotes vasculogenesis by activation of VEGF/PI3K/Akt pathway.
Front Biosci (Landmark Ed)
PUBLISHED: 06-05-2014
Show Abstract
Hide Abstract
Knowledge about factors regulating vasculogenesis remains limited. The cellular repressor of E1A-stimulated gene (CREG) has been reported to be involved in maintaining cellular differentiation and endothelial homeostasis, thus we hypothesize that CREG may be a novel factor regulating vasculogenesis. By using mouse embryonic stem cells (ESC) derived embryoid body (EB) model, we confirmed expression of CREG was significantly up-regulated during EB differentiation. Overexpression of CREG in ESC led to accelerated cystic EB formation, increased endothelial differentiation and vasculogenesis, whereas knockdown of CREG produced opposite phenotypes. Moreover, we found expression of vascular endothelial growth factor (VEGF) was up-regulated and PI3K/Akt pathway was activated in CREG-overexpressing EB. Administration of VEGF neutralizing antibody or PI3K/Akt pharmacological inhibitor LY294002 blocked the vasculogenesis in CREG over-expressing EB, while supplement of VEGF rescued vasculogenesis deficiency in CREG knocked down EB. Further study by Western blot determined that PI3K/Akt was a downstream effector of VEGF. We identify CREG as a novel factor in regulating endothelial differentiation and vasculogenesis via VEGF/PI3K/Akt pathway.
Related JoVE Video
CREG1 promotes angiogenesis and neovascularization.
Front Biosci (Landmark Ed)
PUBLISHED: 06-05-2014
Show Abstract
Hide Abstract
Angiogenesis has long been considered as an important strategy for ischemic injury. It has been reported that cellular repressor of E1A-stimulated genes (CREG1) promotes human umbilical vein endothelial cell (HUVEC) proliferation, migration, and protects endothelial cell (EC) from apoptosis. However, its potential effect on angiogenesis remains undefined. In the present study, we investigated the role and mechanisms of CREG1 in promoting angiogenesis. We found that adenovirus-transduced CREG1 expression in HUVECs increases EC tube formation in matrigel and promotes neovascularization in matrigel plugs grafted into wild type mice. In addition, adenoviral CREG1 expression enhances filopodia formation, which is accompanied by increased expression of integrin-linked kinase (ILK) and activation of its downstream effector Cdc42. Hindlimb perfusion was significantly reduced after femoral artery ligation in CREG1 heterozygous knockout mice. Finally, adenoviral CREG1 was injected intramuscularly in gastrochemius and partially restores ischemic hindlimb perfusion. Our results demonstrated that CREG1 increases EC filopodia formation and vascular assembly via ILK-Cdc42 activation and promotes neovascularization, which might be a therapeutic target for ischemic injury.
Related JoVE Video
Enhanced production of nitric oxide in A549 cells through activation of TRPA1 ion channel by cold stress.
Nitric Oxide
PUBLISHED: 04-19-2014
Show Abstract
Hide Abstract
The respiratory epithelium is exposed to the external environment, and inhalation of cold air is common during the season of winter. In addition, the lung is a major source of nitric oxide (NO). However, the effect of cold stress on the production of NO is still unclear. In the present work, We measured the change of NO in single cell with DACF-DA and the change in cytosolic Ca(2+) concentration ([Ca(2+)]c) in A549 cell. We observed that cold stress (from 20 °C to 5 °C) induced an increase of NO in A549 cell, which was completely abolished by applying an extracellular Ca(2+) free medium. Further experiments showed that cold-sensing transient receptor potential subfamily member 1 (TRPA1) channel agonist (allyl isothiocyanate, AITC) increased the production of NO and the level of [Ca(2+)]c in A549 cell. Additionally, TRPA1 inhibitor, Ruthenium red (RR) and camphor, significantly blocked the enhanced production of NO and the rise of [Ca(2+)]c induced by AITC or cold stimulation, respectively. Taken together, these data indicated that cold-induced TRPA1 activation was responsible for the enhanced production of NO in A549 cell.
Related JoVE Video
Clinical feasibility and safety of a novel miniature mobile cardiac catheterization laboratory in diagnosis and treatment for coronary heart disease.
Chin. Med. J.
PUBLISHED: 03-14-2014
Show Abstract
Hide Abstract
The lack of medical facilities causes delayed diagnosis and treatment of coronary heart disease in remote mountainous area and/or at disaster site. The miniature mobile cardiac catheterization laboratory was developed to be an intervention platform for coronary heart disease diagnosis and treatment by our team. Pre-clinical research indicated that the miniature mobile cardiac catheterization laboratory performed well in the rescue of critical cardiovascular diseases, even ST-segment elevation myocardial infarction. The present study aimed to evaluate the clinical safety and timeliness of the miniature mobile cardiac catheterization laboratory for emergent coronary interventional diagnosis and treatment.
Related JoVE Video
Hospital quality improvement initiative for patients with acute coronary syndromes in China: a cluster randomized, controlled trial.
Circ Cardiovasc Qual Outcomes
PUBLISHED: 03-11-2014
Show Abstract
Hide Abstract
Background- Substantial evidence-practice gaps exist in the management of acute coronary syndromes (ACS) in China. Clinical pathways are tools for improving ACS quality of care but have not been rigorously evaluated. Methods and Results- Between October 2007 and August 2010, a quality improvement program was conducted in 75 hospitals throughout China with mixed methods evaluation in a cluster randomized, controlled trial. Eligible hospitals were level 2 or level 3 centers routinely admitting >100 patients with ACS per year. Hospitals were assigned immediate implementation of the American Heart Association/American College of Cardiology guideline based clinical pathways or commencement of the intervention 12 months later. Outcomes were several key performance indicators reflecting the management of ACS. The key performance indicators were measured 12 months after commencement in intervention hospitals and compared with baseline data in control hospitals, using data collected from 50 consecutive patients in each hospital. Pathway implementation was associated with an increased proportion of patients discharged on appropriate medical therapy, with nonsignificant improvements or absence of effects on other key performance indicators. Conclusions- Among hospitals in China, the use of a clinical pathway for the treatment of ACS compared with usual care improved secondary prevention treatments, but effectiveness was otherwise limited. An accompanying process evaluation identified several health system barriers to more successful implementation. Clinical Trial Registration- URL: http://www.anzctr.org.au/default.aspx. Unique identifier: ACTRN12609000491268.
Related JoVE Video
Effects of intracoronary sodium nitroprusside compared with adenosine on fractional flow reserve measurement.
J Invasive Cardiol
PUBLISHED: 03-11-2014
Show Abstract
Hide Abstract
The purpose of this study was to compare the efficacy and safety of intracoronary (IC) sodium nitroprusside (SNP) and IC adenosine (AD) for fractional flow reserve (FFR) measurement. We compared the FFR response and side effect profiles of IC AD and IC SNP in 40 patients with a combined total of 53 moderate coronary stenoses. Boluses of AD at doses of 40 ?g (A1) and 60 ?g (A2), and SNP at doses of 0.3 ?g/kg (S1), 0.6 ?g/kg (S2), and 0.9 ?g/kg (S3) were used to achieve coronary hyperemia. The mean FFR value decreased significantly by 7.96% (A1), 10.51% (A2), 8.74% (S1), 10.58% (S2), and 10.73% (S3) compared with the baseline distal coronary pressure/aortic pressure. IC SNP delayed the mean time to peak value of FFR by 87.5%, 79.0%, and 88.6% in S1, S2, and S3, respectively, compared with A2 (P<.001). The mean duration of the plateau phase was longer in S1 (50.47 ± 14.25 s), S2 (51.33 ± 16.41 s) and S3 (57.60 ± 18.07 s) compared with A2 (27.93 ± 11.90 s; P<.01). IC AD caused shortness of breath in 11 patients (27.5%), flushing in 4 patients (10%), headache in 8 patients (20%), and transient second-degree atrioventricular block (AVB) in 6 patients (15%). IC SNP may be used as a hyperemic agent in FFR measurements. It may be preferable to IC AD as a routine clinical stimulus and has the additional advantage of showing a longer plateau phase.
Related JoVE Video
A prospective, multicenter, randomized trial of paclitaxel-coated balloon versus paclitaxel-eluting stent for the treatment of drug-eluting stent in-stent restenosis: results from the PEPCAD China ISR trial.
JACC Cardiovasc Interv
PUBLISHED: 02-22-2014
Show Abstract
Hide Abstract
The intention of the PEPCAD China ISR (A Prospective, Multicenter, Randomized Trial of Paclitaxel-Coated versus Paclitaxel-Eluting Stent for the Treatment of Drug-Eluting Stent In-Stent Restenosis) was to demonstrate the efficacy of paclitaxel-coated balloon (PCB) angioplasty in a non-European patient population with coronary drug-eluting stent in-stent restenosis (DES-ISR).
Related JoVE Video
Dietary salt intake and coronary atherosclerosis in patients with prehypertension.
J Clin Hypertens (Greenwich)
PUBLISHED: 02-16-2014
Show Abstract
Hide Abstract
High dietary salt intake is known to contribute to hypertension and cardiovascular and cerebrovascular diseases. The authors investigated the association between dietary salt intake and development of hypertension or cardiovascular disease (CVD) in 243 patients with prehypertension. After a median follow-up of 4.53 years (range, 3.1-8.7), 123 (50.6%) patients developed hypertension and 71 (29.2%) experienced cardiovascular events, including fatal and nonfatal myocardial infarctions. Adjusted hazard ratios for patients with a high salt diet (?6 g/d) were 1.57 (95% confidence interval [CI], 1.17-3.31; P=.018) for hypertension and 1.97 (95% CI, 1.08-2.27; P=.011) for CVD. Multivariable-adjusted analyses of subgroups showed a significant association between salt intake and CVD, but no such association was found in patients younger than 60 years, women, or patients with normal weight or normal cholesterol level. These results provide further research of prevention of hypertension and CVD in prehypertension.
Related JoVE Video
Remodeling of small intramyocardial coronary arteries distal to total occlusions after myocardial infarction in pigs.
Coron. Artery Dis.
PUBLISHED: 08-01-2013
Show Abstract
Hide Abstract
The present study was designed to investigate whether microvascular remodeling could occur in hibernating myocardium and infarction regions distal to a total occluded coronary artery after acute myocardial infarction.
Related JoVE Video
Simultaneous Determination of Two Epimeric Furofuran Lignans (Sesamin and Asarinin) of Asarum heterotropoides Extract in Rat Plasma by LC/MS/MS: Application to Pharmacokinetic Study.
J Chromatogr Sci
PUBLISHED: 07-25-2013
Show Abstract
Hide Abstract
A rapid, sensitive and selective liquid chromatography-tandem mass spectrometry was developed to determine two epimeric furofuran lignans (sesamin and asarinin) simultaneously from Asarum heterotropoides extract in rat plasma. Simple protein precipitation with acetonitrile was performed to extract analytes by using alantolactone as an internal standard. Chromatographic separation was achieved using a DIKMA Diamonsil C18 analytical column (4.6 mm × 150 mm, i.d., 5 µm) by isocratically eluting with a mobile phase consisting of methanol/5 mM ammonium acetate/formic acid (75:25:0.1, v/v/v) at a flow rate of 0.8 mL/min. Tandem mass spectrometric detection with an electrospray ionization interface was performed by multiple reaction monitoring in positive ionization mode. This method was validated according to specificity, sensitivity, linearity, intra- and inter-day precision (<10.7%) and accuracy (<2.3%) and recovery and stability in a concentration range of 25.0-15 000 ng/mL for sesamin and 5.00-3 000 ng/mL for asarinin. This method has been successfully applied in a pharmacokinetic study of A. heterotropoides extract containing sesamin and asarinin after this extract was orally administrated in rats.
Related JoVE Video
CREG promotes the proliferation of human umbilical vein endothelial cells through the ERK/cyclin E signaling pathway.
Int J Mol Sci
PUBLISHED: 06-25-2013
Show Abstract
Hide Abstract
Cellular repressor of E1A-stimulated genes (CREG) is a recently discovered secreted glycoprotein involved in homeostatic modulation. We previously reported that CREG is abundantly expressed in the adult vascular endothelium and dramatically downregulated in atherosclerotic lesions. In addition, CREG participates in the regulation of apoptosis, inflammation and wound healing of vascular endothelial cells. In the present study, we attempted to investigate the effect of CREG on the proliferation of vascular endothelial cells and to decipher the underlying molecular mechanisms. Overexpression of CREG in human umbilical vein endothelial cells (HUVEC) was obtained by infection with adenovirus carrying CREG. HUVEC proliferation was investigated by flow cytometry and 5-bromo-2-deoxy-uridine (BrdU) incorporation assays. The expressions of cyclins, cyclin-dependent kinases and signaling molecules were also examined. In CREG-overexpressing cells, we observed a marked increase in the proportion of the S and G2 population and a decrease in the G0/G1 phase population. The number of BrdU positively-stained cells also increased, obviously. Furthermore, silencing of CREG expression by specific short hairpin RNA effectively inhibited the proliferation of human umbilical vein endothelial cells (HUVEC). CREG overexpression induced the expression of cyclin E in both protein and mRNA levels to regulate cell cycle progression. Further investigation using inhibitor blocking analysis identified that ERK activation mediated the CREG modulation of the proliferation and cyclin E expression in HUVEC. In addition, blocking vascular endothelial growth factor (VEGF) in CREG-overexpressed HUVEC and supplementation of VEGF in CREG knocked-down HUVEC identified that the pro-proliferative effect of CREG was partially mediated by VEGF-induced ERK/cyclin E activation. These results suggest a novel role of CREG to promote HUVEC proliferation through the ERK/cyclin E signaling pathway.
Related JoVE Video
SU6668 suppresses proliferation of triple negative breast cancer cells through down-regulating MTDH expression.
Cancer Cell Int.
PUBLISHED: 06-25-2013
Show Abstract
Hide Abstract
The multiple tyrosine kinase inhibitors SU6668 have a promising therapeutic effect on the progression of hematological malignancies and some solid tumors. Here, we determined its effect on triple negative breast cancer (TNBC) cells and explored the potential molecular mechanism.
Related JoVE Video
Cellular repressor of E1A stimulated genes enhances endothelial monolayer integrity.
Mol. Biol. Rep.
PUBLISHED: 04-12-2013
Show Abstract
Hide Abstract
Cellular repressor of E1A stimulated genes (CREG) is a novel modulator that maintains the homeostasis of vascular cells. The present study aimed to investigate the effects of CREG on tumor necrosis factor (TNF)-?-mediated inflammatory injury of vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were cultured and CREG overexpressing (VC), knockdown (VS) and mock-transfected (VE) HUVECs were challenged with TNF-?. We demonstrated that TNF-? prompted robust intercellular filamentous actin (F-actin) stress fiber formation as examined by rhodamin-phalloidin staining. Transwell assay and rhodamine B isothiocyanate-dextran staining indicated that TNF-? induced intercellular hyperpermeability of the HUVEC monolayers. These effects were attenuated in VC cells with forced CREG overexpression but significantly potentiated in VS cells with CREG silencing. After TNF-? stimulation, interleukin (IL)-6 and IL-8 secretions in VE cells were markedly increased and inducible nitric oxidase (iNOS) expression substantially elevated, whereas these effects were pronouncedly damped in VC cells. Conversely, in VS cells, the increase in inflammatory markers was substantially potentiated. Immunofluorescence staining demonstrated that nuclear factor ?B (NF-?B) slowly and transiently translocated into the nuclei of VC cells upon TNF-? stimulation. However, a more swift and sustained nuclear translocation was observed in VS as compared to VE cells. Corresponding changes in the pattern of its protein expression was also observed. These data suggested that CREG can inhibit NF-?B activation, TNF-?-induced inflammatory responses and the hyperpermeability of endothelial cells, and may therefore represent a potential therapeutic target for pathological vascular injury.
Related JoVE Video
Short-Term Rosuvastatin Therapy for Prevention of Contrast-Induced Acute Kidney Injury in Patients with Diabetes and Chronic Kidney Disease.
J. Am. Coll. Cardiol.
PUBLISHED: 03-15-2013
Show Abstract
Hide Abstract
The aim of this study was to evaluate the safety and efficacy of rosuvastatin inpreventing Contrast-induced acute kidney injury (CIAKI) in patients with diabetes mellitus(DM) and chronic kidney disease(CKD).
Related JoVE Video
Nanoporous CREG-eluting stent attenuates in-stent neointimal formation in porcine coronary arteries.
PLoS ONE
PUBLISHED: 03-01-2013
Show Abstract
Hide Abstract
The goal of this study was to evaluate the efficacy of a nanoporous CREG-eluting stent (CREGES) in inhibiting neointimal formation in a porcine coronary model.
Related JoVE Video
Related JoVE Video
Association between the -786T>C 1polymorphism in the promoter region of endothelial nitric oxide synthase (eNOS) and risk of coronary artery disease: A systematic review and meta-analysis.
Gene
PUBLISHED: 02-16-2013
Show Abstract
Hide Abstract
A variety of studies have evaluated the association between the -786T>C polymorphism in the promoter region of endothelial nitric oxide synthase (eNOS) and risk of coronary artery disease (CAD). However, the results remain conflicting. To better understand the role of eNOS -786T>C polymorphism in CAD risk, we conducted a comprehensive systematic review and meta-analysis.
Related JoVE Video
Rosuvastatin enhances the therapeutic efficacy of adipose-derived mesenchymal stem cells for myocardial infarction via PI3K/Akt and MEK/ERK pathways.
Basic Res. Cardiol.
PUBLISHED: 01-24-2013
Show Abstract
Hide Abstract
The poor viability of transplanted stem cells hampers their therapeutic efficacy for treatment of myocardial infarction. The aim of this study was to investigate whether rosuvastatin improved survival of adipose-derived mesenchymal stem cells (AD-MSCs) after transplantation into infarcted hearts. AD-MSCs isolated from Tg(Fluc-egfp) mice which constitutively express both firefly luciferase (Fluc) and enhanced green fluorescent protein were transplanted into infarcted hearts with or without rosuvastatin administration. Longitudinal in vivo bioluminescence imaging and histological staining revealed that rosuvastatin enhanced the survival of engrafted AD-MSCs. Furthermore, combined therapy of AD-MSC and rosuvastatin reduced fibrosis, decreased cardiomyocyte apoptosis, and preserved heart function. AD-MSCs were then subjected to hypoxia and serum deprivation injury in vitro to mimic the ischemic environment. Rosuvastatin (10(-6) mmol/L) enhanced the viability and paracrine effect of AD-MSCs, and decreased their apoptotic rate. Western blotting revealed that rosuvastatin supplementation increased Akt and ERK phosphorylation, which resulted in FoxO3a phosphorylation and nuclear export. In addition, rosuvastatin administration decreased the pro-apoptotic proteins Bim and Bax, and increased the anti-apoptotic proteins Bcl-xL and Bcl-2. Furthermore, these effects were abolished by PI3K inhibitor LY294002 and MEK1/2 inhibitor U0126. This study demonstrates that rosuvastatin may improve the survival of engrafted AD-MSCs at least in part through the PI3K/Akt and MEK/ERK1/2 signaling pathways. Combination therapy with rosuvastatin and AD-MSCs has a synergetic effect on improving myocardial function after infarction.
Related JoVE Video
Long-term clinical effects of programmer-guided atrioventricular and interventricular delay optimization: Intracardiac electrography versus echocardiography for cardiac resynchronization therapy in patients with heart failure.
J. Int. Med. Res.
PUBLISHED: 01-23-2013
Show Abstract
Hide Abstract
To compare the haemodynamic results and long-term clinical outcomes of intracardiac electrography (QuickOpt®; St Jude Medical, St Paul, MN, USA) and echocardiography for optimization of atrioventricular (AV) and interventricular (VV) delays in cardiac resynchronization therapy (CRT).
Related JoVE Video
A new atlas localization approach for subthalamic nucleus utilizing Chinese visible human head datasets.
PLoS ONE
PUBLISHED: 01-18-2013
Show Abstract
Hide Abstract
To study the possibility of Chinese visible human (CVH) head datasets as brain atlas for locating the subthalamic nucleus (STN) before deep brain stimulation (DBS) surgery.
Related JoVE Video
Protective Effects of Mesenchymal Stem Cells with CXCR4 Up-Regulation in a Rat Renal Transplantation Model.
PLoS ONE
PUBLISHED: 01-01-2013
Show Abstract
Hide Abstract
The homing of mesenchymal stem cells to injured tissue, which is important for the correction of conditions such as ischemia-reperfusion injury (IRI) and immunolesions, has been performed previously, but with poor efficiency. Substantial improvements in engraftment are required to derive clinical benefits from MSC transplantation. Chemokines are the most important factors that control cellular migration. Stromal derived factor-1 (SDF-1) is up-regulated during tissue/organ ischemia damage, and its cognate receptor, chemokine receptor 4 (CXCR4), is involved in stem cell migration. The aim of our study was to investigate CXCR4 expression in MSCs and to validate both its role in mediating migration to transplanted kidneys and its immunoregulatory effects in renal protection. Specifically, the present study was designed to investigate the short-term tissue homing of MSCs carrying genetically modified CXCR4 in a rat renal transplantation model. We tested the hypothesis that MSCs with CXCR4 over-expression can more efficiently regulate immunological reactions. Lentiviral vectors were used to over-express CXCR4 or to introduce a short hairpin ribonucleic acid (shRNA) construct targeting endogenous CXCR4 in rat MSCs. MSCs were labeled with enhanced green fluorescent protein (eGFP). After cell sorting, recipient kidneys were regionally perfused; recipient animals were injected with transduced MSCs, native MSCs, or PBS via tail vein following renal transplantation; and the effects of MSC injection were observed.
Related JoVE Video
Electrophysiological characteristics of focal atrial tachycardia surrounding the aortic coronary cusps.
Circ Arrhythm Electrophysiol
PUBLISHED: 10-10-2011
Show Abstract
Hide Abstract
Catheter ablation of atrial tachycardia (AT) arising near the coronary cusps has been reported in limited numbers of patients. We investigated the electrophysiological characteristics of these ATs in 22 consecutive patients.
Related JoVE Video
Translational research on novel drug-eluting stents in percutaneous coronary intervention.
Front Med
PUBLISHED: 09-16-2011
Show Abstract
Hide Abstract
Although first-generation drug-eluting stents (DES) have markedly reduced restenosis, complications of late and very late in-stent thrombosis have emerged as prime limitations to this technology. The development of new DES is a key process to prevent these complications. Translational research plays a very important role in experiments which determine the safety and efficacy of DES before human clinical trials. The present review focuses on translational research of novel DES, including drug discovery, creation of preclinical research models, planning and conducting of first-in-man studies, and developing next-generation DES systems.
Related JoVE Video
Percutaneous transluminal intervention and antiplatelet therapy following endovascular graft exclusion for Stanford B thoracic aortic dissection.
Int. J. Cardiol.
PUBLISHED: 07-16-2011
Show Abstract
Hide Abstract
To evaluate the safety and feasibility of percutaneous coronary intervention and antiplatelet therapy in patients who have undergone endovascular graft exclusion.
Related JoVE Video
Cdc42 controls vascular network assembly through protein kinase C? during embryonic vasculogenesis.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 06-09-2011
Show Abstract
Hide Abstract
The goal of this study was to determine the role of Cdc42 in embryonic vasculogenesis and the underlying mechanisms.
Related JoVE Video
Cellular repressor of E1A-stimulated genes regulates vascular endothelial cell migration by the ILK/AKT/mTOR/VEGF(165) signaling pathway.
Exp. Cell Res.
PUBLISHED: 05-16-2011
Show Abstract
Hide Abstract
The migration of vascular endothelial cells plays a critical role in a variety of vascular physiological and pathological processes, such as embryonic development, angiogenesis, wound healing, re-endothelialization, and vascular remodeling. This study clarified the role and mechanism of a new vascular homeostasis regulator, Cellular repressor of E1A-stimulated genes (CREG), in the migration of primary human umbilical vein endothelial cells (HUVECs). A wound healing assay and transwell migration model showed that upregulation of CREG expression induced HUVEC migration and it was positively correlated with the expression of vascular endothelial growth factor. Furthermore, wild type integrin-linked kinase reversed the poor mobility of CREG knock-down HUVECs; in contrast, kinase-dead integrin-linked kinase weakened the migration of HUVECs. We also studied the effect of CREG on HUVEC migration by the addition of an mTOR inhibitor, recombinant vascular endothelial growth factor(165), neutralizing antibody of vascular endothelial growth factor(165) and AKT siRNA, and we concluded that CREG induces endothelial cell migration by activating the integrin-linked kinase/AKT/mTOR/VEGF(165) signaling pathway.
Related JoVE Video
Interleukin-8 gene polymorphism is associated with acute coronary syndrome in the Chinese Han population.
Cytokine
PUBLISHED: 03-21-2011
Show Abstract
Hide Abstract
Acute coronary syndrome (ACS) is one of the most common forms of heart disease. Recent studies have shown that interleukin (IL)-8 plays a key role in the development of atherosclerotic plaques, but the relationship between the common genetic variants of IL-8 and ACS has not been extensively studied.
Related JoVE Video
Sustained clinical safety and efficacy of a biodegradable-polymer coated sirolimus-eluting stent in "real-world" practice: three-year outcomes of the CREATE (Multi-Center Registry of EXCEL Biodegradable Polymer Drug Eluting Stents) study.
Catheter Cardiovasc Interv
PUBLISHED: 03-07-2011
Show Abstract
Hide Abstract
The CREATE is a post-marketing surveillance multicenter registry that demonstrated satisfactory angiographic and clinical (at 18 months) outcomes of a biodegradable polymer based sirolimus-eluting stent (EXCEL, JW Medical System, Weihai, China) for the treatment of patients in routine clinical practice.
Related JoVE Video
Overexpression of CREG attenuates atherosclerotic endothelium apoptosis via VEGF/PI3K/AKT pathway.
Atherosclerosis
PUBLISHED: 01-22-2011
Show Abstract
Hide Abstract
Cellular repressor of E1A-stimulated genes (CREG) is a homeostasis-modulating gene abundantly expressed in adult artery endothelium. Previous studies have demonstrated a protective effect of CREG against atherosclerosis through prevention of vascular smooth muscle cell apoptosis. However, the role of CREG in endothelial cells (ECs) apoptosis and the underlying signaling mechanisms are unknown.
Related JoVE Video
Glycosylation-independent binding to extracellular domains 11-13 of mannose-6-phosphate/insulin-like growth factor-2 receptor mediates the effects of soluble CREG on the phenotypic modulation of vascular smooth muscle cells.
J. Mol. Cell. Cardiol.
PUBLISHED: 11-30-2010
Show Abstract
Hide Abstract
The bio-effects of cellular repressor of E1A-stimulated genes (CREG) have been proposed to depend on its N-glycosylation and binding to mannose-6-phosphate/insulin-like growth factor-2 receptor (M6P/IGF2R). The present study aimed to investigate the detailed mode and specific sites for their binding and the functional relevance of this binding in the phenotypic modulation of vascular smooth muscle cells (SMCs). Wild-type and glycosylation mutant human CREG (wtCREG and mCREG) proteins were expressed and isolated from HEK293 cells. CREG knocked-down SMCs were used to evaluate their biological activity. Both wtCREG and mCREG arrest cell cycle progression of CREG knocked-down SMCs when added to the culture medium. In vitro binding assay revealed that CREG bound to M6P/IGF2R extracellular domains 7-10 and 11-13 in a glycosylation-dependent and -independent manner, respectively. Further blocking experiments using soluble M6P/IGF2R fragments and M6P/IGF2R neutralizing antibody suggest that the binding to domains 11-13, as well as to 7-10, is adequate for CREG to modulate SMC proliferation. These data suggest that soluble CREG protein can exert its biological function via glycosylation-independent binding to the extracellular domains 11-13 of cell surface M6P/IGF2R, and thereby provide novel insights into CREG modulation of SMC phenotypic switching from contractile to proliferative.
Related JoVE Video
Suppression of encephalitogenic T-cell responses by cilostazol is associated with upregulation of regulatory T cells.
Neuroreport
PUBLISHED: 05-18-2010
Show Abstract
Hide Abstract
Cilostazol is a specific phosphodiesterase III inhibitor. Recent data show that cilostazol has anti-inflammatory effects and administration of cilostazol ameliorates experimental autoimmune encephalomyelitis (EAE). In this study, we used a mouse EAE model to explore the role of cilostazol in Th1 and Th17 cell-mediated immune responses. We found that cilostazol suppressed mitogen or antigen-induced T-cell responses and Th17 cell differentiation in vitro, which correlated with enhanced Treg-cell responses. Beginning of oral administration of cilostazol at the onset of EAE significantly inhibited encephalitogenic T cells, reduced the levels of inflammatory cytokines in the central nervous system, and ameliorated the severity of EAE. Moreover, administration of cilostazol markedly enhanced Treg-cell response in vivo. Cilostazol, therefore, may exert its therapeutic effects through upregulation of Treg-cell activity.
Related JoVE Video
Interleukin-17A gene variants and risk of coronary artery disease: a large angiography-based study.
Clin. Chim. Acta
PUBLISHED: 05-14-2010
Show Abstract
Hide Abstract
Recent studies have also revealed that interleukin (IL)-17A plays a key role in atherosclerosis and its complication, but the relationship of its common variants with coronary artery disease (CAD) has not been extensively studied. We systematically screened sequence variations in the IL17A gene and designed an angiography-based case-controlled study consisting of 1031 CAD patients and 935 control subjects to investigate the association between the selected polymorphisms of IL-17A gene and CAD risk in Chinese Han population. Frequencies of IL17A rs8193037 GG homozygote and G allele were significantly higher in the patient group than those in the control group (P<0.001; OR=0.68; 95% CI=0.54-0.85). Stratification analysis showed that the IL17A rs8193037 G allele significantly increased the risk of CAD only among male subjects (P=0.001; OR=0.63; 95% CI=0.47-0.83). After adjustment for conventional risk factors, binary logistic regression analysis showed that the G allele carriers (GG+AG) had significantly increased CAD risk compared with the AA homozygotes (adjusted P<0.001; OR 0.43; 95% CI, 0.33-0.58). ELISA showed augmented IL17A production in plasma of the AMI patients. Based on our data, we speculated that the SNP rs8193037 of IL17A gene is significantly associated with CAD risk in Chinese Han population and the rs8193037 G allele which is associated with increased expression of IL17A in AMI patients may be an independent predictive factor for CAD.
Related JoVE Video
Rac1 is essential for basement membrane-dependent epiblast survival.
Mol. Cell. Biol.
PUBLISHED: 05-10-2010
Show Abstract
Hide Abstract
During murine peri-implantation development, the egg cylinder forms from a solid cell mass by the apoptotic removal of inner cells that do not contact the basement membrane (BM) and the selective survival of the epiblast epithelium, which does. The signaling pathways that mediate this fundamental biological process are largely unknown. Here we demonstrate that Rac1 ablation in embryonic stem cell-derived embryoid bodies (EBs) leads to massive apoptosis of epiblast cells in contact with the BM. Expression of wild-type Rac1 in the mutant EBs rescues the BM-contacting epiblast, while expression of a constitutively active Rac1 additionally blocks the apoptosis of inner cells and cavitation, indicating that the spatially regulated activation of Rac1 is required for epithelial cyst formation. We further show that Rac1 is activated through integrin-mediated recruitment of the Crk-DOCK180 complex and mediates BM-dependent epiblast survival through activating the phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. Our results reveal a signaling cascade triggered by cell-BM interactions essential for epithelial morphogenesis.
Related JoVE Video
A novel method to inhibit apoptosis and promote differentiation of induced pluripotent stem cells in transplantation therapy for myocardial infarction.
Med. Hypotheses
PUBLISHED: 04-20-2010
Show Abstract
Hide Abstract
Myocardial ischemic disorders are the leading causes of mortality worldwide, and current therapies only delay progression of these diseases. Traditional stem cell therapies face various impediments, including the typical ethical and immunological problems in clinical application. Recently, induced pluripotent stem (iPS) cells have been shown to offer a novel fascinating route to patient-specific and disease-specific pluripotent cells, without the technical and ethical limitations of somatic cell nuclear transfer method. However, iPS cells limited viability after transplantation in infarcted microenvironment, and low rate of differentiation into cardiovascular tissues restricts their regenerative capacity. Genetically modified iPS cells with the recently discovered cellular repressor of E1A-stimulated genes (CREG), which inhibits apoptosis and inflammation but enhances differentiation, may resolve these crucial problems. Possible mechanisms may include CREG promotion of angiogenesis by VEGF, suppression of inflammation and resistance of apoptosis via activating PI3K/Akt and blocking p38 MARK signaling, and maintenance of endothelial differentiation conditions. The exact mechanisms that CREG can modulate iPS cells survival and differentiation remain to be investigated.
Related JoVE Video
Prognostic effects of pulmonary hypertension in patients undergoing cardiac resynchronization therapy.
J Thorac Dis
PUBLISHED: 04-14-2010
Show Abstract
Hide Abstract
Aim of this study is to investigate the impact of elevated pulmonary artery systolic pressure (PASP) on mortality and the clinical outcome after cardiac resynchronization therapy (CRT).
Related JoVE Video
Lack of association between cellular repressor of E1A-stimulated genes (CREG) [corrected] polymorphisms and coronary artery disease in the Han population of North China.
Clin. Chim. Acta
PUBLISHED: 03-22-2010
Show Abstract
Hide Abstract
Phenotypic switching of smooth muscle cells (SMCs) plays a critical role in the pathogenesis of atherosclerotic lesions such as coronary artery disease (CAD). Accumulating evidence demonstrates that a cellular repressor of E1A-stimulated genes (CREG) plays a role in the maintenance of the mature phenotype of vascular SMCs. We assessed the possible association between CREG and CAD in the Han population of North China.
Related JoVE Video
Pattern of expression of the CREG gene and CREG protein in the mouse embryo.
Mol. Biol. Rep.
PUBLISHED: 01-20-2010
Show Abstract
Hide Abstract
The cellular repressor of E1A-stimulated genes (CREG) is a secreted glycoprotein that inhibits cell proliferation and/or enhances differentiation. CREG is widely expressed in adult tissues such as the brain, heart, lungs, liver, intestines and kidneys in mice. We investigated the level of CREG expression during mouse embryogenesis and its distribution at 18.5 days post coitus (dpc) using immunohistochemical staining with diaminobenzidine, western blotting and reverse transcription-polymerase chain reaction. CREG expression was first detected in mouse embryos at 4.5 dpc. It was expressed at almost all stages up to 18.5 dpc. The level of CREG was found to increase gradually and was highest at 18.5 dpc. Western blotting showed that the CREG protein was expressed at higher levels in the brain, heart, intestines and kidneys than in the lungs and liver at 18.5 dpc. In 9.5 dpc embryos, CREG was expressed only in the endothelial cells of blood vessels, after the vascular lumen had formed. With advanced differentiation, vascular smooth muscle cells developed in the embryonic vascular structures; the expression of smooth muscle ?-actin protein and CREG were positive and increased gradually in 10.5 dpc embryonic vessels. CREG expression in the embryonic blood vessels peaked at 15.5 dpc and was reduced slightly at 18.5 dpc. These results indicate that CREG is expressed during mouse embryogenesis and might participate in the differentiation of these organs during embryogenesis.
Related JoVE Video
Cellular repressor of E1A-stimulated genes inhibits human vascular smooth muscle cell apoptosis via blocking P38/JNK MAP kinase activation.
J. Mol. Cell. Cardiol.
PUBLISHED: 01-06-2010
Show Abstract
Hide Abstract
Vascular smooth muscle cell (VSMC) apoptosis accelerates atherosclerosis and promotes restenosis following vascular injury. The current study examined the effects of cellular repressor of E1A-stimulated genes (CREG), a novel glycoprotein inhibiting transcription activation, on the regulation of VSMC apoptosis. Serum starvation or treatment of human VSMCs with apoptosis inducers (STS or VP-16) significantly reduced CREG expression and caused caspase-3 activation. CREG downregulation and caspase-3 activation were inversely related, suggesting that reduced CREG expression may contribute to VSMC apoptosis. Both loss-of-function (CREG-DW produced by retroviruses expressing CREG shRNAs) and gain-of-function (CREG-UP produced by retroviral infection with vector pLNCX-CREG) studies were performed to confirm this hypothesis. CREG-DW significantly increased VSMC apoptosis, whereas CREG-UP significantly reduced apoptosis. Moreover, p38 and JNK mitogen-activated protein kinases were significantly upregulated in CREG-DW and significantly reduced in CREG-UP VSMCs. More importantly, CREG-DW-induced VSMC apoptosis was blocked by the p38-specific inhibitor SB203580 or by overexpression of a dominant-negative P38 alpha (p38 alpha AGF). Balloon injury-induced vascular caspase-3 activation was significantly inhibited by treatment with recombinant CREG protein. These results demonstrated for the first time that CREG plays a key role in modulating VSMC apoptosis through the p38 and JNK signal transduction pathways, both in vitro and in situ.
Related JoVE Video
Association analysis of the IL-17F His161Arg polymorphism in myocardial infarction.
Coron. Artery Dis.
PUBLISHED: 10-20-2009
Show Abstract
Hide Abstract
There is growing evidence that coronary atherosclerosis and its most severe phenotype, myocardial infarction (MI), are chronic inflammatory diseases. Interleukins are important mediators and modulators of inflammation. The His161Arg polymorphism in the gene encoding of IL-17F has recently been consistently found to be associated with chronic inflammatory disorders. In this study, we explored the hypothesis that the variant also affects the risk of MI.
Related JoVE Video
An intron polymorphism in the CXCL16 gene is associated with increased risk of coronary artery disease in Chinese Han population: a large angiography-based study.
Atherosclerosis
PUBLISHED: 06-16-2009
Show Abstract
Hide Abstract
Experimental and clinical observations suggest that CXCL16, a recently discovered transmembrane chemokine combining functions of a chemokine and a scavenger receptor, could be an important player in atherosclerosis, but the relationship of its common variants with coronary artery disease (CAD) has not been extensively studied.
Related JoVE Video
Safety and efficacy of biodegradable polymer-coated sirolimus-eluting stents in "real-world" practice: 18-month clinical and 9-month angiographic outcomes.
JACC Cardiovasc Interv
PUBLISHED: 05-26-2009
Show Abstract
Hide Abstract
This study sought to evaluate the safety and efficacy of a biodegradable polymer-coated sirolimus-eluting stent (Excel, JW Medical System, Weihai, China) with 6-month dual antiplatelet therapy in daily practice.
Related JoVE Video
Endogenous transforming growth factor (TGF) beta1 promotes differentiation of smooth muscle cells from embryonic stem cells: stable plasmid-based siRNA silencing of TGF beta1 gene expression.
J Physiol Sci
PUBLISHED: 03-25-2009
Show Abstract
Hide Abstract
Transforming growth factor (TGF) beta1 has been shown to promote differentiation of smooth muscle cells (SMC) from some precursor cells. Whether endogenous TGF beta1 also contributes to SMC differentiation during embryogenesis, however, remains unclear. In this study, a plasmid-based TGF beta1 RNA interference embryonic stem (ES) cell line was constructed. Morphological observation showed that TGF beta1 knockdown significantly prevented differentiated cells from outgrowing from ES cells-derived embryoid bodies (EBs). Immunofluorescence staining indicated that SM alpha-actin-positive cells were confluent and dense in the control group but dispersed in the TGF beta1 knockdown group. RT-PCR and western blot suggested that TGF beta1 knockdown resulted in a decrease in the expression of early SMC markers SM alpha-actin and myocardin in EBs. Both the retarded extension of cell outgrowth and the decrease in SM alpha-actin and myocardin expression could not be rescued by addition of exogenous TGF beta1. These data suggest that endogenous TGF beta1 promotes differentiation of SMC from ES cells.
Related JoVE Video
Association of interleukin-18 gene promoter polymorphisms with risk of acute myocardial infarction in northern Chinese Han population.
Clin. Chem. Lab. Med.
PUBLISHED: 03-25-2009
Show Abstract
Hide Abstract
Interleukin-18 (IL-18) has been suggested to play an important role in coronary arterial disease and its sequelae. The aim of the present study was to investigate the association between IL-18 promoter functional polymorphisms (-607C/A and -137G/C) and acute myocardial infarction (AMI) in northern Chinese Han population.
Related JoVE Video
CREG inhibits migration of human vascular smooth muscle cells by mediating IGF-II endocytosis.
Exp. Cell Res.
PUBLISHED: 03-19-2009
Show Abstract
Hide Abstract
We previously determined that the cellular repressor of E1A-stimulated genes, (CREG) plays a role in the maintenance of the mature phenotype of vascular smooth muscle cells (SMCs). This study aimed to identify the role of CREG in modulating the migration of SMCs. Recombinant virus-mediated CREG expression inhibited the cellular migration of cultured SMCs associated with down-regulated activity of matrix metalloproteinase-9 (MMP-9). In contrast, CREG knockdown via the retroviral transfer of short hairpin RNAs promoted cellular migration. Enzyme-linked immunosorbent assay and endocytosis analysis revealed that CREG knockdown attenuated the internalization and increased secretion of insulin-like growth factor (IGF)-II. Western blot analysis demonstrated that both phosphoinositide 3-kinase (PI3K) and phosphatase Akt were enhanced in CREG knockdown SMCs. Furthermore, the effect of CREG knockdown on SMC migration was abrogated in a dose-dependent manner by the addition of either IGF-II neutralizing antibody or the PI3K inhibitor, LY294002. These results indicate that the CREG knockdown-mediated increase in IGF-II secretion promoted cellular migration in SMCs via the PI3K/Akt signal pathway. Additionally, blockage of IGF-II binding to the mannose-6-phosphate/IGF-II receptor (M6P/IGF2R) by IGF2R antibody or recombinant IGF2R fragment attenuated the endocytosis of IGF-II in cells overexpressing CREG. This indicates that M6P/IGF2R is involved in the regulation of CREG-mediated IGF-II endocytosis. In summary, these data demonstrate for the first time that CREG plays a critical role in the inhibition of SMC migration, as well as maintaining SMCs in a mature phenotype. These results may provide a new therapeutic target for vascular disease associated with neointimal hyperplasia.
Related JoVE Video
A monocyte chemoattractant protein-1 gene polymorphism is not associated with coronary artery disease in a Han Chinese population.
Clin. Chim. Acta
PUBLISHED: 02-03-2009
Show Abstract
Hide Abstract
Coronary artery disease (CAD) is one of the most common forms of heart diseases. Monocyte chemoattractant protein-1 gene (MCP-1, CCL2) has been considered one of the candidate genes that play a role in atherogenesis of CAD. Recently, the association of a single nucleotide polymorphism (SNP) in the MCP-1 gene promoter (-2518A>G) and CAD has been investigated with controversial results.
Related JoVE Video
Cilostazol in addition to aspirin and clopidogrel improves long-term outcomes after percutaneous coronary intervention in patients with acute coronary syndromes: a randomized, controlled study.
Am. Heart J.
PUBLISHED: 01-06-2009
Show Abstract
Hide Abstract
Cilostazol has been widely used to prevent peripheral vascular events, and its antiplatelet mechanisms may different from aspirin and clopidogrel. We hypothesized that cilostazol in addition to aspirin and clopidogrel effectively reduces systemic ischemic events after percutaneous coronary intervention (PCI) in high-risk patients.
Related JoVE Video
Comparison of long-term efficacy of the paclitaxel-eluting stent versus the bare-metal stent for treatment of unprotected left main coronary artery disease.
Am. J. Cardiol.
PUBLISHED: 01-06-2009
Show Abstract
Hide Abstract
The use of paclitaxel-eluting stents (PES) for the treatment of unprotected left main coronary artery (LMCA) disease is controversial. Between January 2003 and December 2006, a total of 287 patients undergoing percutaneous coronary intervention for LMCA lesions were consecutively registered. Of those patients, 178 received PES and 109 received bare-metal stents (BMS). Estimated perioperative mortality rates were 7.3% and 6.8% for the BMS and PES groups, respectively (p=0.51). PES recipients had distal left main bifurcation lesions more frequently compared with BMS recipients (72 vs 42%, p<0.01). At an average follow-up of 35 months, the rates of major adverse cardiac events (4.5 vs 23.9%, adjusted odds ratio [OR] 0.23, 95% confidence interval [CI] 0.09 to 0.58, p<0.001) and target-lesion revascularization (2.2 vs 13.8%, adjusted OR 0.26, 95% CI 0.08 to 0.83, p<0.001) were significantly lower in the PES group than in the BMS group. Overall thrombotic event rates were 1.1% and 4.6% in the PES and BMS groups, respectively (p=0.08). Angiographic follow-up was performed in 61% and 59% of PES and BMS recipients, respectively. The angiographic restenosis rate was significantly lower in the PES group as compared with the BMS group (3.7 vs 23.4%, p<0.001). In conclusion, PES implantation provides a safe, effective therapy for unprotected LMCA disease and decreases the risk of major adverse cardiac events compared with BMS at a mean follow-up of 35 months.
Related JoVE Video
Angiotensin-converting enzyme I/D polymorphism and the risk of thoracic aortic dissection in Chinese Han population.
Mol. Biol. Rep.
Show Abstract
Hide Abstract
Thoracic aortic dissection (TAD) is a catastrophic cardiovascular disease and is thought to have a genetic basis. Various studies have indicated that renin-angiotensin system plays an important role in the pathogenesis of aortic disease. To determine the association of the I/D polymorphism of ACE gene with the risk of TAD in a Chinese Han population, a hospital-based case-control study was designed consisting of 161 subjects with TAD and 256 control subjects. The genotype frequency of the ACE I/D polymorphism was determined by using a polymerase chain reaction assay. The overall distribution of ACE I/D genotypes was significantly different between the two groups. Compared with the controls, the frequency of DD genotypes and the D allele of ACE gene were significantly increased in TAD patients. Multivariate logistic regression adjusting for conventional vascular risk factors confirmed the association between the ACE I/D polymorphism and the susceptibility to TAD (OR 2.14, 95 % CI 1.38-3.32, P = 0.001). Our data demonstrated that the ACE I/D polymorphism appeared to be an important risk factor in the development of TAD. However, further validation in large population-based studies is needed to confirm the finding.
Related JoVE Video
Adipose stromal cell and sarpogrelate orchestrate the recovery of inflammation-induced angiogenesis in aged hindlimb ischemic mice.
Aging Cell
Show Abstract
Hide Abstract
Aging population displays a much higher risk of peripheral arterial disease (PAD) possibly due to the higher susceptibility, poor prognosis, and fewer therapeutic options. This study was designed to examine the impact of combined multipotent adipose-derived stromal cells (mADSCs) and sarpogrelate treatment on aging hindlimb ischemia and the mechanism of action involved. mADSCs (1.0 × 10(7)) constitutively expressing enhanced green fluorescent protein (eGFP) or firefly luciferase (Fluc) reporter were engrafted into the hindlimb of aged Vegfr2-luc transgenic or FVB/N mice subjected to unilateral femoral artery occlusion, followed by a further administration of sarpogrelate. Multimodality molecular imaging was employed to noninvasively evaluate mADSCs survival and therapeutic efficacy against aging hindlimb ischemia. Aged Tg(Vegfr2-luc) mice exhibited decreased inflammatory response, and downregulation of vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor-2 (VEGFR2) compared with young ones following hindlimb ischemia induction, resulting in angiogenesis insufficiency and decompensation for ischemia recovery. Engrafted mADSCs augmented inflammation-induced angiogenesis to yield pro-angiogenic/anti-apoptotic effects partly via the VEGF/VEGFR2/mTOR/STAT3 pathway. Nonetheless, mADSCs displayed limited survival and efficacy following transplantation. Sarpogrelate treatment with mADSCs further upregulated mammalian target of rapamycin (mTOR)/STAT3 signal and modulated pro-/anti-inflammatory markers including IL-1?/TNF-?/IFN-? and IL-6/IL-10, which ultimately facilitated mADSCs survival and therapeutic benefit in vivo. Sarpogrelate prevented mADSCs from hypoxia/reoxygenation-induced cell death via a mTOR/STAT3-dependent pathway in vitro. This study demonstrated a role of in vivo kinetics of VEGFR2 as a biomarker to evaluate cell-derived therapeutic angiogenesis in aging. mADSCs and sarpogrelate synergistically restored impaired angiogenesis and inflammation modulatory capacity in aged hindlimb ischemic mice, indicating its therapeutic promise for PAD in the elderly.
Related JoVE Video
Cellular repressor E1A-stimulated genes controls phenotypic switching of adventitial fibroblasts by blocking p38MAPK activation.
Atherosclerosis
Show Abstract
Hide Abstract
Phenotypic modulation of adventitial fibroblasts (AFs) plays an important role in the pathogenesis of proliferative vascular diseases. The current study aimed to identify the role of cellular repressor E1A-stimulated genes (CREG), a critical mediator in the maintenance of vascular homeostasis, in AF phenotypic modulation and adventitial remodeling.
Related JoVE Video
Bnip3 and AIF cooperate to induce apoptosis and cavitation during epithelial morphogenesis.
J. Cell Biol.
Show Abstract
Hide Abstract
Apoptosis is an essential step in cavitation during embryonic epithelial morphogenesis, but its mechanisms are largely unknown. In this paper, we used embryonic stem cell-differentiated embryoid bodies (EBs) as a model and found that Bnip3 (Bcl-2/adenovirus E1B 19-kD interacting protein), a BH3-only proapoptotic protein, was highly up-regulated during cavitation in a hypoxia-dependent manner. Short hairpin RNA silencing of Bnip3 inhibited apoptosis of the core cells and delayed cavitation. We show that the Bnip3 up-regulation was mediated mainly by hypoxia-inducible factor (HIF)-2. Ablation of HIF-2? or HIF-1?, the common ? subunit of HIF-1 and -2, suppressed Bnip3 up-regulation and inhibited apoptosis and cavitation. We further show that apoptosis-inducing factor (AIF) cooperated with Bnip3 to promote lumen clearance. Bnip3 silencing in AIF-null EBs nearly blocked apoptosis and cavitation. Moreover, AIF also regulated Bnip3 expression through mitochondrial production of reactive oxygen species and consequent HIF-2? stabilization. These results uncover a mechanism of cavitation through hypoxia-induced apoptosis of the core cells mediated by HIFs, Bnip3, and AIF.
Related JoVE Video
Association of ALOX5AP haplotypes with susceptibility to coronary artery disease in a Chinese Han population.
Eur. J. Intern. Med.
Show Abstract
Hide Abstract
The 5-lipoxygenase activating protein (FLAP), encoded by the activating 5-lipoxygenase (ALOX5AP) gene, is a crucial mediator of the biosynthesis of leukotrienes, which have been implicated in atherosclerosis. This study investigates whether ALOX5AP polymorphisms are associated with coronary artery disease (CAD) in a Chinese Han population.
Related JoVE Video

What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.