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Find video protocols related to scientific articles indexed in Pubmed.
[The cytokine homeostasis was regulated by over-expression of Sirt1 in collagen-induced arthritis mice].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
PUBLISHED: 10-02-2014
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Objective To investigate the effects of over-expression of Sirt1 on cytokines in the collagen type 2-induced arthritis (CIA) mice. Methods The female DBA/1 mouse CIA model was establised by subcutaneous injection of collagen type 2. Recombinant adenovirus carrying Sirt1 gene was infected into CIA mice through tail vein injection. The effects of over-expression of Sirt1 on CIA mice were assessed by measuring arthritis index. The serum levels of cytokines including interleukin 1? (IL-1?), tumor necrosis factor ? (TNF-?), IL-17, IL-4 and IL-10 in CIA mice were examined by ELISA. The mRNA levels of Sirt1, matrix metalloproteinase-13 (MMP-13) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were detected by real-time quantitative PCR (qRT-PCR). The protein levels of NF-?B subunit p65 and acetylated p65 were determined by Western blotting. Results Compared with control groups, over-expression of Sirt1 significantly ameliorated the symptoms of arthritis in CIA mouse. Furthermore, proinflammatory factors (IL-1?, TNF-?, IL-17) decreased while anti-inflammatory factors (IL-4 and IL-10) increased in CIA mice. The over-expression of Sirt1 significantly down-regulated MMP-13 mRNA level and up-regulated TIMP-1 mRNA level. Additionally, the over-expressed Sirt1 reduced acetylation of p65. Conclusion Over-expression of Sirt1 may regulate the balance of cytokines in CIA mice.
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Leptin restores the insulinotropic effect of exenatide in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and high-fat diet.
Am. J. Physiol. Endocrinol. Metab.
PUBLISHED: 08-26-2014
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Leptin may reduce pancreatic lipid deposition, which increases with progression of obesity and can impair ?-cell function. The insulinotropic effect of glucagon-like peptide-1 (GLP-1) and the efficacy of GLP-1 receptor agonist are reduced associated with impaired ?-cell function. In this study, we examined whether leptin could restore the efficacy of exenatide, a GLP-1 receptor agonist, in type 2 diabetes with increased adiposity. We chronically administered leptin (500 ?g·kg(-1)·day(-1)) and/or exenatide (20 ?g·kg(-1)·day(-1)) for 2 wk in a mouse model of type 2 diabetes with increased adiposity induced by streptozotocin and high-fat diet (STZ/HFD mice). The STZ/HFD mice exhibited hyperglycemia, overweight, increased pancreatic triglyceride level, and reduced glucose-stimulated insulin secretion (GSIS); moreover, the insulinotropic effect of exenatide was reduced. However, leptin significantly reduced pancreatic triglyceride level, and adding leptin to exenatide (LEP/EX) remarkably enhanced GSIS. These results suggested that the leptin treatment restored the insulinotropic effect of exenatide in the mice. In addition, LEP/EX reduced food intake, body weight, and triglyceride levels in the skeletal muscle and liver, and corrected hyperglycemia to a greater extent than either monotherapy. The pair-feeding experiment indicated that the marked reduction of pancreatic triglyceride level and enhancement of GSIS by LEP/EX occurred via mechanisms other than calorie restriction. These results suggest that leptin treatment may restore the insulinotropic effect of exenatide associated with the reduction of pancreatic lipid deposition in type 2 diabetes with increased adiposity. Combination therapy with leptin and exenatide could be an effective treatment for patients with type 2 diabetes with increased adiposity.
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Study of weathering effects on the distribution of aromatic steroid hydrocarbons in crude oils and oil residues.
Environ Sci Process Impacts
PUBLISHED: 08-22-2014
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The composition and distribution of triaromatic steroid hydrocarbons in oil residues after biodegradation and photo-oxidation processes were detected, and the diagnostic ratios for oil spill identification were developed and evaluated based on the relative standard deviation (RSD) and the repeatability limit. The preferential loss of C27 methyl triaromatic steranes (MTAS) relative to C28 MTAS and C29 MTAS was shown during the photo-oxidation process. In contrast to the photochemical degradation, the MTAS with the original 20R biological configuration was preferentially degraded during the biodegradation process. The RSD of most of the diagnostic ratios of MTAS ranged from 9 to 84% during the photo-oxidation process. However, the RSDs of such ratios derived from MTAS were all <5% even in high biodegradation, and such parameters may also provide new methods on oil spill identification. The parameters of monoaromatic sterane and monoaromatic sterane are not used well for oil spill identification after photo-oxidation. The triaromatic steroid hydrocarbons retained their molecular compositions after biodegradation and photo-oxidation and most of the diagnostic ratios derived from them could be efficiently used in oil spill identification.
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Investigations into the bovine serum albumin binding and fluorescence properties of Tb (III) complex of a novel 8-hydroxyquinoline ligand.
Spectrochim Acta A Mol Biomol Spectrosc
PUBLISHED: 08-09-2014
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A novel ligand, 2-methyl-6-(8-quinolinyl)-dicarboxylate pyridine (L), and its corresponding Tb (III) complex, Na4Tb(L)2Cl4·3H2O, were successfully prepared and characterized. The luminescence spectra showed that the ligand L was an efficient sensitizer for Tb (III) luminescence. The interaction of the complex with bovine serum albumin (BSA) was investigated through fluorescence spectroscopy under physiological conditions. The Stern-Volmer analysis indicated that the fluorescence quenching was resulted from static mechanism. The binding sites (n) approximated 1.0 and this meant that interaction of Na4Tb(L)2Cl4·3H2O with BSA had single binding site. The results showed van der Waals interactions and hydrogen bonds played major roles in the binding reaction. Furthermore, circular dichroism (CD) spectra indicated that the conformation of BSA was changed.
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Inhibition of N-myc downstream-regulated gene-2 is involved in an astrocyte-specific neuroprotection induced by sevoflurane preconditioning.
Anesthesiology
PUBLISHED: 05-29-2014
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Mechanism of sevoflurane preconditioning-induced cerebral ischemic tolerance is unclear. This study investigates the role of N-myc downstream-regulated gene-2 (NDRG2) in the neuroprotection of sevoflurane preconditioning in ischemic model both in vivo and in vitro.
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Critical illness-related corticosteroid insufficiency after multiple traumas: a multicenter, prospective cohort study.
J Trauma Acute Care Surg
PUBLISHED: 05-24-2014
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Given that the observed prevalence and time course of critical illness-related corticosteroid insufficiency (CIRCI) remain inconsistent in trauma patients, the present study was designed to investigate the prevalence, time course, and effect of CIRCI on the outcome of critically ill patients with multiple injuries.
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Use of bio-mimetic three-dimensional technology in therapeutics for heart disease.
Bioengineered
PUBLISHED: 01-14-2014
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Due to the limited self-renewal capacity of cardiomyocytes, the mammalian heart exhibits impaired regeneration and insufficient ability to restore heart function after injury. Cardiovascular tissue engineering is currently considered as a promising alternative therapy to restore the structure and function of the failing heart. Recent evidence suggests that the epicardium may play critical roles in regulation of myocardial development and regeneration. One of the mechanisms that has been proposed for the restorative effect of the epicardium is the specific physiomechanical cues that this layer provides to the cardiac cells. In this article we explore whether a new generation of epicardium-mimicking, acellular matrices can be utilized to enhance cardiac healing after injury. The matrix consists of a dense collagen scaffold with optimized biomechanical properties approaching those of embryonic epicardium. Grafting the epicardial patch onto the ischemic myocardium--promptly after the incidence of infarct--resulted in preserved contractility, attenuated ventricular remodeling, diminished fibrosis, and vascularization within the injured tissue in the adult murine heart.
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The Leu72Met polymorphism of the GHRL gene prevents the development of diabetic nephropathy in Chinese patients with type 2 diabetes mellitus.
Mol. Cell. Biochem.
PUBLISHED: 08-06-2013
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The preproghrelin (GHRL) Leu72Met polymorphism (rs 696217) is associated with obesity, reduced glucose-induced insulin secretion in healthy or diabetic subjects, and reduced serum creatinine (Scr) levels in type 2 diabetes. We evaluated the association of the Leu72Met polymorphism with measures of insulin sensitivity in non-diabetic control individuals and type 2 diabetics, and whether this variation contributes to the development of diabetic nephropathy (DN) in type 2 diabetes. A case-control study was performed of 291 non-diabetic control subjects and 466 patients with type 2 diabetes, of whom 238 had DN with overt albuminuria (DN group; albuminuric excretion rate [AER] ? 300 mg/24 h) and 228 did not have DN, but had diabetes for more than 10 years (non-DN group). Genotyping was performed using a TaqMan PCR assay. The Leu/Leu, Leu/Met, and Met/Met genotype frequencies were significantly different between the non-DN and DN groups (p = 0.011). The frequency of the variant genotypes (Leu/Met, Met/Met) was significantly lower in the DN group than the non-DN group (23.5 vs. 36.0 %, p = 0.003). Met/Met non-diabetic control subjects had lower BMI and Scr levels and higher eGFR level than Leu/Leu or Leu/Met individuals (p < 0.05). Leu/Met and Met/Met type 2 diabetics had significantly lower AER and Scr levels and higher eGFR level than Leu/Leu type 2 diabetics (all p < 0.001). The GHRL Leu72Met polymorphism may help to maintain normal renal function and may protect against the development of DN by reducing albuminuria and improving renal function in Chinese patients with type 2 diabetes.
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Deletion of the ?2-adrenergic receptor prevents the development of cardiomyopathy in mice.
J. Mol. Cell. Cardiol.
PUBLISHED: 07-22-2013
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Beta adrenergic receptor (?-AR) subtypes act through diverse signaling cascades to modulate cardiac function and remodeling. Previous in vitro studies suggest that ?1-AR signaling is cardiotoxic whereas ?2-AR signaling is cardioprotective, and may be the case during ischemia/reperfusion in vivo. The objective of this study was to assess whether ?2-ARs also play a cardioprotective role in the pathogenesis of non-ischemic forms of cardiomyopathy. To dissect the role of ?1 vs ?2-ARs in modulating MLP (Muscle LIM Protein) cardiomyopathy, we crossbred MLP-/- with ?1-/- or ?2-/- mice. Deletion of the ?2-AR improved survival, cardiac function, exercise capacity and myocyte shortening; by contrast haploinsufficency of the ?1-AR reduced survival. Pathologic changes in Ca(2+) handling were reversed in the absence of ?2-ARs: peak Ca(2+) and SR Ca(2+) were decreased in MLP-/- and ?1+/-/MLP-/- but restored in ?2-/-MLP-/-. These changes were associated with reversal of alterations in troponin I and phospholamban phosphorylation. Gi inhibition increased peak and baseline Ca(2+), recapitulating changes observed in the ?2-/-/MLP-/-. The L-type Ca(2+) blocker verapamil significantly decreased cardiac function in ?2-/-MLP-/- vs WT. We next tested if the protective effects of ?2-AR ablation were unique to the MLP model using TAC-induced heart failure. Similar to MLP, ?2-/- mice demonstrated delayed progression of heart failure with restoration of myocyte shortening and peak Ca(2+) and Ca(2+) release. Deletion of ?2-ARs prevents the development of MLP-/- cardiomyopathy via positive modulation of Ca(2+) due to removal of inhibitory Gi signaling and increased phosphorylation of troponin I and phospholamban. Similar effects were seen after TAC. Unlike previous models where ?2-ARs were found to be cardioprotective, in these two models, ?2-AR signaling appears to be deleterious, potentially through negative regulation of Ca(2+) dynamics.
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The effect of bioengineered acellular collagen patch on cardiac remodeling and ventricular function post myocardial infarction.
Biomaterials
PUBLISHED: 07-18-2013
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Regeneration of the damaged myocardium is one of the most challenging fronts in the field of tissue engineering due to the limited capacity of adult heart tissue to heal and to the mechanical and structural constraints of the cardiac tissue. In this study we demonstrate that an engineered acellular scaffold comprising type I collagen, endowed with specific physiomechanical properties, improves cardiac function when used as a cardiac patch following myocardial infarction. Patches were grafted onto the infarcted myocardium in adult murine hearts immediately after ligation of left anterior descending artery and the physiological outcomes were monitored by echocardiography, and by hemodynamic and histological analyses four weeks post infarction. In comparison to infarcted hearts with no treatment, hearts bearing patches preserved contractility and significantly protected the cardiac tissue from injury at the anatomical and functional levels. This improvement was accompanied by attenuated left ventricular remodeling, diminished fibrosis, and formation of a network of interconnected blood vessels within the infarct. Histological and immunostaining confirmed integration of the patch with native cardiac cells including fibroblasts, smooth muscle cells, epicardial cells, and immature cardiomyocytes. In summary, an acellular biomaterial with specific biomechanical properties promotes the endogenous capacity of the infarcted myocardium to attenuate remodeling and improve heart function following myocardial infarction.
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Contributions of leukocyte angiotensin-converting enzyme to development of atherosclerosis.
Arterioscler. Thromb. Vasc. Biol.
PUBLISHED: 07-11-2013
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This study determined the role of angiotensin-converting enzyme (ACE) on the development of angiotensin I-induced atherosclerosis and the contribution of leukocyte-specific expression of this enzyme.
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Dynamic localization and functional implications of C-peptide might for suppression of iNOS in high glucose-stimulated rat mesangial cells.
Mol. Cell. Endocrinol.
PUBLISHED: 06-18-2013
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Although C-peptide has unique beneficial effects on diabetic nephropathy (DN), its functional localization and molecular mechanism have not been fully clarified. Whether C-peptide exhibits its protective role through the regulation of inducible nitric oxide synthase (iNOS), a key enzyme in oxidative stress, is not clear. In this study, it was revealed that C-peptide could enter the nucleus of high glucose-stimulated mesangial cells, especially in a time-dependent manner by high glucose pretreatment, while no C-peptide was detected in low glucose-cultured mesangial cells. The dynamic functional localization of C-peptide might be the intrinsic cause of its unique beneficial effects for DN, which may provide a foundation for further clarification of its underlying mechanism. Our preliminarily data also shown C-peptide suppressed the iNOS expression. Taking together, these results revealed the dynamic functional localization of C-peptide by high glucose stimulation in rat mesangial cells, which might suppress expression of iNOS to exhibit its protective effects.
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Mutations in KCNJ11 are associated with the development of autosomal dominant, early-onset type 2 diabetes.
Diabetologia
PUBLISHED: 06-01-2013
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More than 90% of Chinese familial early-onset type 2 diabetes mellitus is genetically unexplained. To investigate the molecular aetiology, we identified and characterised whether mutations in the KCNJ11 gene are responsible for these families.
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Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure.
Am. J. Physiol. Heart Circ. Physiol.
PUBLISHED: 05-31-2013
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Alterations in the ubiquitin-proteasome system (UPS) have been described in left ventricular hypertrophy and failure, although results have been inconsistent. The role of the UPS in right ventricular (RV) hypertrophy (RVH) and RV failure (RVF) is unknown. Given the greater percent increase in RV mass associated with RV afterload stress, as present in many congenital heart lesions, we hypothesized that alterations in the UPS could play an important role in RVH/RVF. UPS expression and activity were measured in the RV from mice with RVH/RVF secondary to pulmonary artery constriction (PAC). Epoxomicin and MG132 were used to inhibit the proteasome, and overexpression of the 11S PA28? subunit was used to activate the proteasome. PAC mice developed RVH (109.3% increase in RV weight to body weight), RV dilation with septal shift, RV dysfunction, and clinical RVF. Proteasomal function (26S ?? chymotrypsin-like activity) was decreased 26% (P < 0.05). Protein expression of 19S subunit Rpt5 (P < 0.05), UCHL1 deubiquitinase (P < 0.0001), and Smurf1 E3 ubiquitin ligase (P < 0.01) were increased, as were polyubiquitinated proteins (P < 0.05) and free-ubiquitins (P = 0.05). Pro-apoptotic Bax was increased (P < 0.0001), whereas anti-apoptotic Bcl-2 decreased (P < 0.05), resulting in a sixfold increase in the Bax/Bcl-2 ratio. Proteasomal inhibition did not accelerate RVF. However, proteasome enhancement by cardiac-specific proteasome overexpression partially improved survival. Proteasome activity is decreased in RVH/RVF, associated with upregulation of key UPS regulators and pro-apoptotic signaling. Enhancement of proteasome function partially attenuates RVF, suggesting that UPS dysfunction contributes to RVF.
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Pharmacokinetics of single and multiple oral doses of arbidol in healthy Chinese volunteers.
Int J Clin Pharmacol Ther
PUBLISHED: 04-18-2013
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Arbidol is licensed in Russia and China for prophylaxis and treatment of influenza A and B. This study was to assess the pharmacokinetics of single and multiple doses of arbidol in healthy Chinese volunteers.
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FK506 activates BMPR2, rescues endothelial dysfunction, and reverses pulmonary hypertension.
J. Clin. Invest.
PUBLISHED: 03-22-2013
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Dysfunctional bone morphogenetic protein receptor-2 (BMPR2) signaling is implicated in the pathogenesis of pulmonary arterial hypertension (PAH). We used a transcriptional high-throughput luciferase reporter assay to screen 3,756 FDA-approved drugs and bioactive compounds for induction of BMPR2 signaling. The best response was achieved with FK506 (tacrolimus), via a dual mechanism of action as a calcineurin inhibitor that also binds FK-binding protein-12 (FKBP12), a repressor of BMP signaling. FK506 released FKBP12 from type I receptors activin receptor-like kinase 1 (ALK1), ALK2, and ALK3 and activated downstream SMAD1/5 and MAPK signaling and ID1 gene regulation in a manner superior to the calcineurin inhibitor cyclosporine and the FKBP12 ligand rapamycin. In pulmonary artery endothelial cells (ECs) from patients with idiopathic PAH, low-dose FK506 reversed dysfunctional BMPR2 signaling. In mice with conditional Bmpr2 deletion in ECs, low-dose FK506 prevented exaggerated chronic hypoxic PAH associated with induction of EC targets of BMP signaling, such as apelin. Low-dose FK506 also reversed severe PAH in rats with medial hypertrophy following monocrotaline and in rats with neointima formation following VEGF receptor blockade and chronic hypoxia. Our studies indicate that low-dose FK506 could be useful in the treatment of PAH.
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Physiologic and molecular characterization of a murine model of right ventricular volume overload.
Am. J. Physiol. Heart Circ. Physiol.
PUBLISHED: 03-15-2013
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Pulmonary insufficiency (PI) is a common long-term sequel after repair of tetralogy of Fallot, causing progressive right ventricular (RV) dilation and failure. We describe the physiologic and molecular characteristics of the first murine model of RV volume overload. PI was created by entrapping the pulmonary valve leaflets with sutures. Imaging, catheterization, and exercise testing were performed at 1, 3, and 6 mo and compared with sham controls. RNA from the RV free wall was hybridized to Agilent whole genome oligonucleotide microarrays. Volume overload resulted in RV enlargement, decreased RV outflow tract shortening fraction at 1 mo followed by normalization at 3 and 6 mo (39 ± 2, 44 ± 2, and 41 ± 2 vs. 46 ± 3% in sham), early reversal of early and late diastolic filling velocities (E/A ratio) followed by pseudonormalization (0.87 ± 0.08, 0.82 ± 0.08, and 0.96 ± 0.08 vs. 1.04 ± 0.03; P < 0.05), elevated end-diastolic pressure (7.6 ± 0.7, 6.9 ± 0.8, and 7 ± 0.5 vs. 2.7 ± 0.2 mmHg; P < 0.05), and decreased exercise duration (26 ± 0.4, 26 ± 1, and 22 ± 1.3 vs. 30 ± 1.1 min; P < 0.05). Subendocardial RV fibrosis was evident by 1 mo. At 1 mo, 372 genes were significantly downregulated. Mitochondrial pathways and G protein-coupled receptor signaling were the most represented categories. At 3 mo, 434 genes were upregulated and 307 downregulated. While many of the same pathways continued to be downregulated, TNF-?, transforming growth factor-?(1) (TGF-?(1)), p53-signaling, and extracellular matrix (ECM) remodeling transitioned from down- to upregulated. We describe a novel murine model of chronic RV volume overload recapitulating aspects of the clinical disease with gene expression changes suggesting early mitochondrial bioenergetic dysfunction, enhanced TGF-? signaling, ECM remodeling, and apoptosis.
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Design, synthesis and biological evaluation of N-sulfonyl homoserine lactone derivatives as inhibitors of quorum sensing in Chromobacterium violaceum.
Molecules
PUBLISHED: 02-20-2013
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A novel series of N-sulfonyl homoserine lactone derivatives 5a-l has been designed, synthesized and evaluated for quorum sensing inhibitory activities towards violacein production. Of the compounds synthesized, compound 5h was found to possess an excellent level of enantiopurity (99.2% e.e.). The results indicated that compounds bearing an ortho substituent on their phenyl ring exhibited excellent levels of inhibitory activity against violacein production. Compounds 5h and 5k in particular, with IC?? values of 1.64 and 1.66 µM, respectively, were identified as promising lead compounds for further structural modification.
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Cloning, characterization and functional analysis of two type 1 diacylglycerol acyltransferases (DGAT1s) from Tetraena mongolica.
J Integr Plant Biol
PUBLISHED: 02-09-2013
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Two cDNAs encoding putative type 1 acyl-CoA: diacylglycerol acyltransferases (DGAT1, EC 2.3.1.20), were cloned from Tetraena mongolica, an extreme xerophyte with high oil content in the stems. The 1 488-bp and 1 485-bp of the open reading frame (ORF) of the two cDNAs, designated as TmDGAT1a and TmDGAT1b, were both predicted to encode proteins of 495 and 494 amino acids, respectively. Southern blot analysis revealed that TmDGAT1a and TmDGAT1b both had low copy numbers in the T. mongolica genome. In addition to ubiquitous expression with different intensity in different tissues, including stems, leaves and roots, TmDGAT1a and TmDGAT1b, were found to be strongly induced by high salinity, drought and osmotic stress, resulting in a remarkable increase of triacylglycerol (TAG) accumulation in T. mongolica plantlets. TmDGAT1a and TmDGAT1b activities were confirmed in the yeast H1246 quadruple mutant (DGA1, LRO1, ARE1, ARE2) by restoring DGAT activity of the mutant host to produce TAG. Overexpression of TmDGAT1a and TmDGAT1b in soybean hairy roots as well as in T. mongolica calli both resulted in an increase in oil content (ranging from 37% to 108%), accompanied by altered fatty acid profiles.
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Fingerprint and weathering characteristics of crude oils after Dalian oil spill, China.
Mar. Pollut. Bull.
PUBLISHED: 01-10-2013
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In an attempt to analyze the chemical characterization of oil residues and examine the suitability of chemical fingerprinting methods in oil spill investigations, multiple parameters sensitive to both sources and degree of weathering were used to characterize oil residues from "7-16" Dalian oil spill, China. Oil residues collected 90 days to 120 days after the spill showed a weathering pattern where significant amounts of light to middle molecular weight normal alkanes were depleted with pristane and phytane as dominant peaks. Diagnostic ratios developed from n-alkane and selected isoprenoids (e.g. Pr/Ph, n-C17/Pr, n-C18/Ph, carbon preference index, LMW/HMW-alkanes ratio), all display obvious changes over weathering time, indicating that these ratios are not valid for oil source identification. Furthermore, the biomarker ratios of hopanes and steranes with relative standard deviations (RSDs) of 0.88-4.08% were useful for source identification even for severely weathered oil residues. In addition, RSD of ?(13)C values of individual n-alkanes in oil residue varied from 0.07% to 0.20%, which suggest that stable carbon isotope profile of n-alkanes can also be a useful tool for tracing the source of an oil spill.
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Iduna protects HT22 cells from hydrogen peroxide-induced oxidative stress through interfering poly(ADP-ribose) polymerase-1-induced cell death (parthanatos).
Cell. Signal.
PUBLISHED: 01-08-2013
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Oxidative stress-induced cell death is common in many neurological diseases. However, the role of poly(ADP-ribose) polymerase-1-induced cell death (parthanatos) has not been fully elucidated. Here, we found that hydrogen peroxide (H2O2) could lead to PARP-1 activation and apoptosis-inducing factor nuclear translocation in a concentration dependent manner. Iduna, as a novel regulator of parthanatos, was also induced by H2O2. Down-regulation of Iduna by genetic ablation promoted H2O2-induced cell damage. Up-regulation of Iduna reduced the loss of mitochondrial potential and ATP and NAD+ production, but did not affect the mitochondrial dysfunction-induced cytochrome c release, increase of Bax/Bcl-2 ratio, and Caspase-9/Caspase-3 activity. In contrast, overexpression of Iduna inhibited activation of PARP-1 and nuclear translocation of AIF. Further study showed that PARP-1 specific inhibitor, DPQ, blocked the protective effect of Iduna against H2O2-induced oxidative stress. Moreover, in the presence of proteasome inhibitor (MG-132) or ubiquitin E1 inhibitor (PYR-41), protective effect of Iduna was significantly weaken. These results indicate that Iduna acts as a potential antioxidant by improving mitochondrial function and inhibiting oxidative stress-induced parthanatos, and these protective effects are dependent on the involvement of ubiquitin-proteasome system.
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CuO-promoted construction of N-2-aryl-substituted-1,2,3-triazoles via azide-chalcone oxidative cycloaddition and post-triazole arylation.
Org. Lett.
PUBLISHED: 12-01-2011
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An efficient one-pot three-component stepwise approach for the synthesis of N-2-aryl-substituted-1,2,3-triazoles has been developed. By using this azide-chalcone oxidative cycloaddition and post-triazole arylation, a series of N-2-aryl-substituted-1,2,3-triazoles are readily prepared under mild conditions in excellent yields and high regioselectivity. Both the catalyst and substrates are readily available.
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Quick and highly efficient copper-catalyzed cycloaddition of organic azides with terminal alkynes.
Org. Biomol. Chem.
PUBLISHED: 10-24-2011
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Good to excellent yields of 1,4-disubstituted 1,2,3-triazoles were obtained within 2-25 min when the Cu(I)-catalyzed azide-alkyne cycloaddition (CuAAC) reaction was carried out under solvent-free conditions, with [Cu(phen)(PPh(3))(2)]NO(3) (1mol%) as the catalyst.
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A novel risperidone-loaded SAIB-PLGA mixture matrix depot with a reduced burst release: effects of solvents and PLGA on drug release behaviors in vitro/in vivo.
J Mater Sci Mater Med
PUBLISHED: 08-28-2011
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The purpose of this study was to develop an in situ forming SAIB (sucrose acetate isobutyrate)-PLGA (poly (d, lactide-co-glycolide)) mixture matrix depot for sustained release of risperidone. The factors affecting the risperidone release kinetics were investigated to obtain further insight into the drug release mechanisms. The burst release in vitro was significantly reduced (4.95%) by using DMSO as solvent. And, increasing the PLGA content from 2 to 10% w/w decreased the initial release from 6.95 to 1.05%. The initial release in vivo decreased with increasing PLGA content (2.0% w/w PLGA, C(max) = 1161.7 ± 550.2 ng ml(-1); 10% w/w PLGA, C(max) = 280.3 ± 98.5 ng ml(-1)). The persistence (AUC(4-20 days)) over 20 days increased from 76.8 ± 20.7 to 362.8 ± 75.0 ng d ml(-1) by inclusion of 10% PLGA compared with the PLGA-free depot. These results demonstrate that the SAIB-PLGA mixture matrix depot could be useful as a sustained delivery system for risperidone.
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Copper-catalyzed synthesis of quinoxalines with o-phenylenediamine and terminal alkyne in the presence of bases.
Org. Lett.
PUBLISHED: 08-01-2011
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A novel way of synthesizing quinoxalines efficiently through cyclization of o-phenylenediamine and terminal alkyne by Cu(II) and bases is developed. This reaction proceeds smoothly to give the products in moderate to good yields.
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THE ROLE OF ?-ADRENERGIC RECEPTORS IN HEART FAILURE: DIFFERENTIAL REGULATION OF CARDIOTOXICITY AND CARDIOPROTECTION.
Prog. Pediatr. Cardiol.
PUBLISHED: 07-19-2011
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?-adrenergic receptor blockers have demonstrated significant survival benefit and have become standard therapy for adults with dilated cardiomyopathy, although their efficacy in pediatric patients is still unproven. Recent data suggests that the two major cardiac ?-adrenergic receptor subtypes (?1 and ?2) couple differentially to intracellular signaling pathways regulating contractility and remodeling. This has led some to suggest that the ?1 receptor is the "cardiotoxic subtype" whereas the ?2 receptor is "cardioprotective." Given this paradigm, there could be situations where subtype selective ?-blockade or even subtype selective ?-stimulation might be beneficial. However, since most of these studies have been performed in isolated cardiomyocytes, their application to clinical practice is unclear. To better understand the roles of ?1- vs. ?2-receptors in the pathogenesis of clinical cardiomyopathy, we and others have taken advantage of several well-characterized murine models of cardiovascular disease. These studies demonstrate that ?-receptor regulation of the balance between cardioprotection and cardiotoxicity is even more complex than previously appreciated: the role of each ?-receptor subtype may vary depending on the specific cardiac stressor involved (e.g. ischemia, pressure overload, genetic mutation, cardiotoxin). Furthermore, the remodeling effects of ?-receptor signaling have a temporal component, depending on whether a cardiac stress is acute vs. chronic.
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Characterization of reference genes for quantitative real-time PCR analysis in various tissues of Anoectochilus roxburghii.
Mol. Biol. Rep.
PUBLISHED: 07-03-2011
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Accurate quantification of transcript profiling with quantitative real time polymerase chain reaction (qRT-PCR) relies on the reliable normalization of an appropriate reference gene. This study reported the identification and validation of nine reference genes, including ?-tubulin (?-TUB), elongation factor 1 alpha (EF-1?), elongation factor 1 beta (EF-1?), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ubiquitin (UBQ), actin 1/2(ACT-1 and ACT-2), 18S rRNA, and 26S rRNA, from Anoectochilus roxburghii (Wall.) Lindl., a valuable herb remedy widely used for various diseases treatment in traditional Chinese medicine. Transcriptional levels of the candidate reference genes were examined using qRT-PCR analysis and revealed differential expression of the genes in the leaf, stem, root, flower, and peduncle tissues. The relative quantities data were subjected to geNorm software for ranking the expression stability of the reference genes and the results showed that EF-1? and ACT-2 were the two best stable genes whereas GAPDH and 26S rRNA did not favor normalization of qRT-PCR in these tissues. The expression pattern of a squalene synthase encoding gene (SS) was also determined in parallel. The analyses were in great consistency when the qRT-PCR data was normalized to the expression of each or both of EF-1? and ACT-2 as the internal control, further confirming the reliability of EF-1? and ACT-2 as the best internal control. The present study provided the first important clues for accurate data normalization in transcript profiling in A. roxburghii, which will be essential to further functional genomics study in the valuable medicinal plant.
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Cardiac pressure overload hypertrophy is differentially regulated by ?-adrenergic receptor subtypes.
Am. J. Physiol. Heart Circ. Physiol.
PUBLISHED: 06-24-2011
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In isolated myocytes, hypertrophy induced by norepinephrine is mediated via ?(1)-adrenergic receptors (ARs) and not ?-ARs. However, mice with deletions of both major cardiac ?(1)-ARs still develop hypertrophy in response to pressure overload. Our purpose was to better define the role of ?-AR subtypes in regulating cardiac hypertrophy in vivo, important given the widespread clinical use of ?-AR antagonists and the likelihood that patients treated with these agents could develop conditions of further afterload stress. Mice with deletions of ?(1), ?(2), or both ?(1)- and ?(2)-ARs were subjected to transverse aortic constriction (TAC). After 3 wk, ?(1)(-/-) showed a 21% increase in heart to body weight vs. sham controls, similar to wild type, whereas ?(2)(-/-) developed exaggerated (49% increase) hypertrophy. Only when both ?-ARs were ablated (?(1)?(2)(-/-)) was hypertrophy totally abolished. Cardiac function was preserved in all genotypes. Several known inhibitors of cardiac hypertrophy (FK506 binding protein 5, thioredoxin interacting protein, and S100A9) were upregulated in ?(1)?(2)(-/-) compared with the other genotypes, whereas transforming growth factor-?(2), a positive mediator of hypertrophy was upregulated in all genotypes except the ?(1)?(2)(-/-). In contrast to recent reports suggesting that angiogenesis plays a critical role in regulating cardiac hypertrophy-induced heart failure, we found no evidence that angiogenesis or its regulators (VEGF, Hif1?, and p53) play a role in compensated cardiac hypertrophy. Pressure overload hypertrophy in vivo is dependent on a coordination of signaling through both ?(1)- and ?(2)-ARs, mediated through several key cardiac remodeling pathways. Angiogenesis is not a prerequisite for compensated cardiac hypertrophy.
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Neutrophil elastase is produced by pulmonary artery smooth muscle cells and is linked to neointimal lesions.
Am. J. Pathol.
PUBLISHED: 03-29-2011
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Previously, we reported that murine gammaherpesvirus-68 (M1-MHV-68) induces pulmonary artery (PA) neointimal lesions in S100A4-overexpressing, but not in wild-type (C57), mice. Lesions were associated with heightened lung elastase activity and PA elastin degradation. We now investigate a direct relationship between elastase and PA neointimal lesions, the nature and source of the enzyme, and its presence in clinical disease. We found an association exists between the percentage of PAs with neointimal lesions and elastin fragmentation in S100A4 mice 6 months after viral infection. Confocal microscopy documented the heightened susceptibility of S100A4 versus C57 PA elastin to degradation by elastase. A transient increase in lung elastase activity occurs in S100A4 mice, 7 days after M1-MHV-68, unrelated to inflammation or viral load and before neointimal lesions. Administration of recombinant elafin, an elastase-specific inhibitor, ameliorates early increases in serine elastase and attenuates later development of neointimal lesions. Neutrophils are the source of elevated elastase (NE) in the S100A4 lung, and NE mRNA and protein levels are greater in PA smooth muscle cells (SMC) from S100A4 mice than from C57 mice. Furthermore, elevated NE is observed in cultured PA SMC from idiopathic PA hypertension versus that in control lungs and localizes to neointimal lesions. Thus, PA SMC produce NE, and heightened production and activity of NE is linked to experimental and clinical pulmonary vascular disease.
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Evaluation of the efficacy, toxicity and safety of vinorelbine incorporated in a lipid emulsion.
Int J Pharm
PUBLISHED: 03-11-2011
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To reduce the severe adverse effects of vinorelbine (VRB) with the aim of improving patient compliance, a parenteral vinorelbine-loaded lipid emulsion (VLE) has been developed. The objective of the present study was to get insight into the preclinical antitumor efficacy, toxicity and safety of VLE, and compare this with that of the commercial product, Navelbine(®) i.v. (VS). Comparable antitumor efficacy of VLE and VS was observed in tumor-bearing nude mouse models inoculated with A549 human lung cancer, hepatoma solidity (Heps) G2 cancer and BCAP-37 human breast cancer cells. The median lethal dose (LD(50)) in mice was 29.3mg/kg (male) and 32.1mg/kg (female) for VLE, while the corresponding value was 30.5mg/kg (male and female) for VS. In the long-term toxicity study, VLE significantly reduced the decreases in RBC, HC, WBC and WBC differential count (DC) levels. Lesions in spleen, thymus, lymph nodes, bone marrow, testis, ovary and injection site induced by VS were much more severe compared with VLE. VLE also exhibited less local venous irritation than VS, as well as no hemolysis or hypersensitivity. Consequently, these observations clearly indicate that the lipid emulsion could be a useful potential parenteral carrier for VRB with equivalent efficacy and lower toxicity.
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?2-adrenergic receptors mediate cardioprotection through crosstalk with mitochondrial cell death pathways.
J. Mol. Cell. Cardiol.
PUBLISHED: 03-09-2011
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?-adrenergic receptors (?-ARs) modulate cardiotoxicity/cardioprotection through crosstalk with multiple signaling pathways. We have previously shown that ?2-ARs are cardioprotective during exposure to oxidative stress induced by doxorubicin (DOX). DOX cardiotoxicity is mediated in part through a Ca(2+)-dependent opening of the mitochondrial permeability transition (MPT), however the signals linking a cell surface receptor like the ?2-AR to regulators of mitochondrial function are not clear. The objective of this study was to assess mechanisms of crosstalk between ?2-ARs and mitochondrial cell death pathways. DOX administered to WT mice resulted in no acute mortality, however 85% of ?2-/- mice died within 30 min. Several pro- and anti-survival pathways were altered. The pro-survival kinase, ?PKC, was decreased by 64% in ?2-/- after DOX vs WT (p<0.01); the ?PKC activator ??RACK partially rescued these mice (47% reduction in mortality). Activity of the pro-survival kinase Akt decreased by 76% in ?2-/- after DOX vs WT (p<0.01). The ?1-antagonist prazosin restored Akt activity to normal and also partially reversed the mortality (45%). Deletion of the ?2-AR increased rate of Ca(2+) release by 75% and peak [Ca(2+)](i) by 20% respectively in isolated cardiomyocytes; the Ca(2+) channel blocker verapamil also partially rescued the ?2-/- (26%). Mitochondrial architecture was disrupted and complex I and II activities decreased by 40.9% and 34.6% respectively after DOX only in ?2-/-. The MPT blocker cyclosporine reduced DOX mortality by 41% and prazosin plus cyclosporine acted synergistically to decrease mortality by 85%. ?2-ARs activate pro-survival kinases and attenuate mitochondrial dysfunction during oxidative stress; absence of ?2-ARs enhances cardiotoxicity via negative regulation of survival kinases and enhancement of intracellular Ca(2+), thus predisposing the mitochondria to opening of the MPT.
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A lyophilized etoposide submicron emulsion with a high drug loading for intravenous injection: preparation, evaluation, and pharmacokinetics in rats.
Drug Dev Ind Pharm
PUBLISHED: 11-06-2010
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To develop a submicron emulsion for etoposide with a high drug loading capacity using a drug-phospholipid complex combined with drug freeze-drying techniques.
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The inhibition effect of high storage temperature on the recrystallization rate during dissolution of nimodipine-Kollidon VA64 solid dispersions (NM-SD) prepared by hot-melt extrusion.
J Pharm Sci
PUBLISHED: 09-30-2010
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Nimodipine (NM) solid dispersions (SD) were prepared by hot-melt extrusion with polyvinylpyrrolidone/vinyl acetate copolymer (PVP-VA; Kollidon VA64) as the carrier, then the extrudate was stored at different temperatures (20°C, 40°C, 60°C) after milling. Conventional differential scanning calorimetry and powder X-ray diffraction revealed that the drug was present as an amorphous state in the carrier. The dissolution curves of NM from SD at 37°C in water showed that the rate of recrystallization for NM from SD stored at high temperatures was slower than that from room temperature. The single glass transition temperature (T(g) ) measured by modulated temperature DSC remained constant around 89°C and indicated that the amorphous state of the compound was not altered by heating. However, the C=O vibration of the amide function of Kollidon VA64 increased from 1658 to 1675 cm(-1) was observed in infrared spectra and implied the weakness of H-bonding between the compound and the polymer. The above-mentioned experiments clued to us that suitable postcooking for a short time is good for SD; however, the mechanisms of the changes were still not clear and need further investigation.
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Evaluation of docetaxel-loaded intravenous lipid emulsion: pharmacokinetics, tissue distribution, antitumor activity, safety and toxicity.
Pharm. Res.
PUBLISHED: 02-05-2010
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The purpose of this study was to carry out a detailed evaluation of an intravenous lipid emulsion for docetaxel (DLE) without Tween 80 before clinical administration.
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Loss of adenomatous poliposis coli-?3 integrin interaction promotes endothelial apoptosis in mice and humans.
Circ. Res.
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Pulmonary hypertension (PH) is characterized by progressive elevation in pulmonary pressure and loss of small pulmonary arteries. As bone morphogenetic proteins promote pulmonary angiogenesis by recruiting the Wnt/?-catenin pathway, we proposed that ?-catenin activation could reduce loss and induce regeneration of small pulmonary arteries (PAs) and attenuate PH.
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Interactions between SIRT1 and MAPK/ERK regulate neuronal apoptosis induced by traumatic brain injury in vitro and in vivo.
Exp. Neurol.
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Traumatic brain injury (TBI) is a serious insult that frequently leads to neurological dysfunction or death. Silent information regulator family protein 1 (SIRT1), as the founding member of nicotinamide adenine dinucleotide (NAD)-dependent deacetylases, has recently been demonstrated to have neuroprotective effect in several models of neurodegenerative diseases. The present study attempts to determine whether SIRT1 has a neuroprotective effect in the model of TBI, and further to investigate the possible regulatory mechanism of neuron death. Thus, we employ transection model in vitro and weight-drop model in vivo to mimic the insults of TBI. The study shows that the expressions of SIRT1, phosphorylation extracellular signal-regulated kinase (p-ERK) and cleaved Caspase-3 are induced after trauma injury in vitro or in vivo. Furthermore, inhibiting SIRT1 by pharmacological inhibitor salermide or SIRT1 siRNA significantly promotes apoptotic neuron death and reduces ERK1/2 activation induced by mechanical injury in vitro and in vivo. Inhibition of ERK1/2 activation with PD98059 or U0126 (two mitogen activated protein kinase kinase inhibitors) in vitro and in vivo significantly attenuates the SIRT1 and cleaved Caspase-3 expression to protect neuron against TBI-induced apoptosis. These results reveal that SIRT1 plays a neuroprotective effect against neuronal apoptosis induced by TBI. The interactions between SIRT1 and MAPK/ERK pathway regulate neuronal apoptosis induced by mechanical trauma injury in vitro and in vivo.
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Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure.
Physiol. Genomics
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MicroRNAs (miRs) are small, noncoding RNAs that are emerging as crucial regulators of cardiac remodeling in left ventricular hypertrophy (LVH) and failure (LVF). However, there are no data on their role in right ventricular hypertrophy (RVH) and failure (RVF). This is a critical question given that the RV is uniquely at risk in patients with congenital right-sided obstructive lesions and in those with systemic RVs. We have developed a murine model of RVH and RVF using pulmonary artery constriction (PAC). miR microarray analysis of RV from PAC vs. control demonstrates altered miR expression with gene targets associated with cardiomyocyte survival and growth during hypertrophy (miR 199a-3p) and reactivation of the fetal gene program during heart failure (miR-208b). The transition from hypertrophy to heart failure is characterized by apoptosis and fibrosis (miRs-34, 21, 1). Most are similar to LVH/LVF. However, there are several key differences between RV and LV: four miRs (34a, 28, 148a, and 93) were upregulated in RVH/RVF that are downregulated or unchanged in LVH/LVF. Furthermore, there is a corresponding downregulation of their putative target genes involving cell survival, proliferation, metabolism, extracellular matrix turnover, and impaired proteosomal function. The current study demonstrates, for the first time, alterations in miRs during the process of RV remodeling and the gene regulatory pathways leading to RVH and RVF. Many of these alterations are similar to those in the afterload-stressed LV. miRs differentially regulated between the RV and LV may contribute to the RVs increased susceptibility to heart failure.
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Protective effect of Homer 1a against hydrogen peroxide-induced oxidative stress in PC12 cells.
Free Radic. Res.
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Oxidative stress-induced cell damage is involved in many neurological diseases. Homer protein, as an important scaffold protein at postsynaptic density, regulates synaptic structure and function. Here, we reported that hydrogen peroxide (H(2)O(2)) induced the expression of Homer 1a. Down-regulation of Homer 1a with a specific small interfering RNA (siRNA) exacerbated H(2)O(2)-induced cell injury. Up-regulation of Homer 1a by lentivirus transfection did not affect the anti-oxidant activity, but significantly reduced the reactive oxygen species (ROS) production and lipid peroxidation after H(2)O(2)-induced oxidative stress. Overexpression of Homer 1a attenuated the loss of mitochondrial membrane potential (MMP) and ATP production induced by H(2)O(2), and subsequently inhibited mitochondrial dysfunction-induced cytochrome c release, increase of Bax/Bcl-2 ratio and caspase-9/caspase-3 activity. Furthermore, in the presence of BAPTA-AM, an intracellular free-calcium (Ca(2+)) chelator, overexpression of Homer 1a had no significant effects on H(2)O(2)-induced oxidative stress. These results suggest that Homer 1a has protective effects against H(2)O(2)-induced oxidative stress by reducing ROS accumulation and activation of mitochondrial apoptotic pathway, and these protective effects are dependent on the regulation of intracellular Ca(2+) homeostasis.
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MFG-E8 activates proliferation of vascular smooth muscle cells via integrin signaling.
Aging Cell
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An accumulation of milk fat globule EGF-8 protein (MFG-E8) occurs within the context of arterial wall inflammatory remodeling during aging, hypertension, diabetes mellitus, or atherosclerosis. MFG-E8 induces VSMC invasion, but whether it affects VSMC proliferation, a salient feature of arterial inflammation, is unknown. Here, we show that in the rat arterial wall in vivo, PCNA and Ki67, markers of cell cycle activation, increase with age between 8 and 30 months. In fresh and early passage VSMC isolated from old aortae, an increase in CDK4 and PCNA, an increase in the acceleration of cell cycle S and G2 phases, decrease in the G1/G0 phase, and an increase in PDGF and its receptors confer elevated proliferative capacity, compared to young VSMC. Increased coexpression and physical interaction of MFG-E8 and integrin ?v?5 occur with aging in both the rat aortic wall in vivo and in VSMC in vitro. In young VSMC in vitro, MFG-E8 added exogenously, or overexpressed endogenously, triggers phosphorylation of ERK1/2, augmented levels of PCNA and CDK4, increased BrdU incorporation, and promotes proliferation, via ?v?5 integrins. MFG-E8 silencing, or its receptor inhibition, or the blockade of ERK1/2 phosphorylation in these cells reduces PCNA and CDK4 levels and decelerates the cell cycle S phase, conferring a reduction in proliferative capacity. Collectively, these results indicate that MFG-E8 in a dose-dependent manner coordinates the expression of cell cycle molecules and facilitates VSMC proliferation via integrin/ERK1/2 signaling. Thus, an increase in MFG-E8 signaling is a mechanism of the age-associated increase in aortic VSMC proliferation.
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C-reactive protein induces interleukin-6 and thrombospondin-1 protein and mRNA expression through activation of nuclear factor-?B in HK-2 cells.
Kidney Blood Press. Res.
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Although C-reactive protein (CRP) is significantly increased in patients with diabetic nephropathy, whether CRP exerts direct proinflammatory effects on human renal tubular epithelial cells (HK-2 cells) is still unclear.
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