continuous-arterial-pressure-monitoring-conscious-rodents-using

Continuous Arterial Pressure Monitoring in Conscious Rodents Using Implantable Telemetry and Comparison with the Tail-Cuff Method

Radio telemetry enables reliable, continuous arterial blood pressure (BP) monitoring in conscious rodents under physiological conditions, while minimizing ...

isolating-ventricular-cardiomyocytes-from-mouse-model-doxorubicin

Isolating Ventricular Cardiomyocytes from a Mouse Model of Doxorubicin Cardiotoxicity

Doxorubicin (DOX) is an effective chemotherapeutic drug whose clinical application is limited by progressive, dose-dependent cardiotoxicity that ...

Dalian Medical University

xi'an jiaotong university

To investigate the dimensional accuracy of digital dental models obtained from the dental cone-beam computed tomography (CBCT) scan of alginate impressions according to the time elapse when the impressions are stored under ambient conditions.

Evaluation of digital dental models obtained from dental cone-beam computed tomography scan of alginate impressions.

Selective deletion of microsomal prostaglandin E synthase-1 (mPges-1) in myeloid cells retards atherogenesis and suppresses the vascular proliferative response to injury, while it does not predispose to thrombogenesis or hypertension. However, studies using bone marrow transplants from irradiated mice suggest that myeloid cell mPGES-1 facilitates cardiac remodeling and prolongs survival after experimental myocardial infarction (MI). Here, we addressed this question using mice lacking mPges-1 in myeloid cells, particularly macrophages [Mac-mPges-1-knockout (KO)], generated by crossing mPges-1 floxed mice with LysMCre mice and subjecting them to coronary artery ligation. Cardiac structure and function were assessed by morphometric analysis, echocardiography, and invasive hemodynamics 3, 7, and 28 days after MI. Despite a similar infarct size, in contrast to the prior report, the post-MI survival rate was markedly improved in the Mac-mPges-1-KO mice compared with wild-type controls. Left ventricular systolic (reflected by ejection fraction, fractional shortness end systolic volume, and +dP/dt) and diastolic function (reflected by end diastolic volume, -dP/dt, and Tau), cardiac hypertrophy (reflected by left ventricular dimensions), and staining for fibrosis did not differ between the groups. In conclusion, we found that Cre-loxP-mediated deletion of mPges-1 in myeloid cells has favorable effects on post-MI survival, with no detectable adverse influence on post-MI remodeling. These results add to evidence that targeting macrophage mPGES-1 may represent a safe and efficacious approach to the treatment and prevention of cardiovascular inflammatory disease.

Myeloid Cell mPges-1 Deletion Attenuates Mortality Without Affecting Remodeling After Acute Myocardial Infarction in Mice.

Circadian rhythms widely exist in living organisms, and they are regulated by the biological clock. Growing evidence has shown that circadian rhythms are tightly related to the physiological function of the cardiovascular system, including blood pressure, heart rate, metabolism of cardiomyocytes, function of endothelial cells, and vasoconstriction and vasodilation. In addition, disruption of circadian rhythms has been considered as one of the important risk factors for cardiovascular diseases, such as myocardial infarction. This review summarizes the recent research advances in the relationship between circadian clock and cardiovascular diseases, hoping to improve treatment strategies for patients with cardiovascular diseases according to the theory of biological clock.

[Research advances in relationship between biological clock and cardiovascular diseases].

Although the molecular components of circadian rhythms oscillate in discrete cellular components of the vasculature and many aspects of vascular function display diurnal variation, the cellular connections between the molecular clock and inflammatory cardiovascular diseases remain to be elucidated. Previously we have shown that pre- versus postnatal deletion of Bmal1 (brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1), the nonredundant core clock gene has contrasting effects on atherogenesis. Here we investigated the effect of myeloid cell Bmal1 deletion on atherogenesis and abdominal aortic aneurysm formation in mice. Approach and Results: Mice lacking Bmal1 in myeloid cells were generated by crossing Bmal1 flox/flox mice with lysozyme 2 promoter-driven Cre recombinase mice on a hyperlipidemic low-density lipoprotein receptor-deficient background and were fed on a high-fat diet to induce atherosclerosis. Atherogenesis was restrained, concomitant with a reduction of aortic proinflammatory gene expression in myeloid cell Bmal1 knockout mice. Body weight, blood pressure, blood glucose, triglycerides, and cholesterol were unaltered. Similarly, myeloid cell depletion of Bmal1 also restrained Ang II (angiotensin II) induced formation of abdominal aortic aneurysm in hyperlipidemic mice. In vitro, RNA-Seq analysis demonstrated a proinflammatory response in cultured macrophages in which there was overexpression of Bmal1.

Bmal1 Deletion in Myeloid Cells Attenuates Atherosclerotic Lesion Development and Restrains Abdominal Aortic Aneurysm Formation in Hyperlipidemic Mice.

Blood pressure (BP) follows a circadian rhythm, it increases on waking in the morning and decreases during sleeping at night. Disruption of the circadian BP rhythm has been reported to be associated with worsened cardiovascular and renal outcomes, however the underlying molecular mechanisms are still not clear. In this review, we briefly summarized the current understanding of the circadian BP regulation and provided therapeutic overview of the relationship between circadian BP rhythm and cardiovascular and renal health and disease.

Circadian Blood Pressure Rhythm in Cardiovascular and Renal Health and Disease.

Procyanidin B2 (PCB2), a natural flavonoid, has been demonstrated to exert anti-oxidation and anti-inflammatory effects on hepatic diseases. Increasing evidence shows the hepatoxicity of nicotine. However, whether PCB2 protects against nicotine-induced hepatoxicity and the underlying mechanisms remains uncharacterized. Here, we reported that nicotine promoted hepatocyte pyroptosis, as evidenced by the elevation of propidium iodide (PI)-positive cells, the activation of Caspase-1 and gasdermin D (GSDMD), the enhanced expression of NOD-like receptor containing pyrin domain 3 (NLRP3) and the increased release of lactate dehydrogenase (LDH), interleukin (IL)-1β and IL-18. The silencing of GSDMD by small interfering RNA (siRNA) efficiently inhibited the release of LDH and the secretion of IL-1β and IL-18. In addition, rosiglitazone (RGZ) prevented hepatocyte pyroptosis induced by nicotine. Furthermore, we showed that PCB2 attenuated nicotine-induced pyroptosis through the activation of peroxisome proliferator-activated receptor-γ (PPARγ) in hepatocytes. Moreover, administration of PCB2 ameliorated liver injury and hepatocyte pyroptosis in nicotine-treated mice. Hence, our findings demonstrated that PCB2 attenuated pyroptosis and liver damage in a PPARγ-dependent manner. Our results suggest a new mechanism by which PCB2 exerts its liver protective effects.

Procyanidin B2 Attenuates Nicotine-Induced Hepatocyte Pyroptosis through a PPARγ-Dependent Mechanism.

Hyperlipidemia with high blood levels of free fatty acids (FFA) is the leading cause of non-alcoholic steatohepatitis. CCN1 is a secreted matricellular protein that drives various cellular functions, including proliferation, migration, and differentiation. However, its role in mediating FFA-induced pro-inflammatory cell death and its underlying molecular mechanisms have not been characterized. In this study, we demonstrated that CCN1 was upregulated in the livers of obese mice. The increase in FFA-induced CCN1 was evaluated in vitro by treating hepatocytes with a combination of oleic acid and palmitic acid (2:1). Gene silencing using specific small interfering RNAs (siRNA) revealed that CCN1 participated in FFA-induced intracellular lipid accumulation, caspase-1 activation, and hepatocyte pyroptosis. Next, we identified integrin αβ as a potential receptor of CCN1. Co-immunoprecipitation demonstrated that the binding between CCN1 and integrin αβ increased in hepatocytes upon FFA stimulation in the livers of obese mice. Similarly, the protein levels of integrin α and β were increased in vitro and in vivo. Experiments with specific siRNAs confirmed that integrin αβ played a part in FFA-induced intracellular lipid accumulation, NLRP3 inflammasome activation, and pyroptosis in hepatocytes. In conclusion, these results provide novel evidence that the CCN1/integrin αβ is a novel mediator that drives hepatic lipotoxicity via NLRP3-dependent pyroptosis.

CCN1/Integrin αβ Instigates Free Fatty Acid-Induced Hepatocyte Lipid Accumulation and Pyroptosis through NLRP3 Inflammasome Activation.

Hyperlipidemia characterized by high blood levels of free fatty acids (FFAs) is important for the progression of inflammatory cardiovascular diseases. Integrin β is a transmembrane receptor that drives various cellular functions, including differentiation, migration, and phagocytosis. However, the underlying mechanisms modifying integrin β protein and activity in mediating monocyte/macrophage adhesion to endothelium remain poorly understood. In this study, we demonstrated that integrin β protein underwent S-nitrosylation in response to nitrosative stress in macrophages. To examine the effect of elevated levels of FFA on the modulation of integrin β expression, we treated the macrophages with a combination of oleic acid and palmitic acid (2:1) and found that FFA activated inducible nitric oxide synthase/nitric oxide and increased the integrin β protein level without altering the mRNA level. FFA promoted integrin β S-nitrosylation via inducible nitric oxide synthase/nitric oxide and prevented its degradation by decreasing binding to E3 ubiquitin ligase c-Cbl. Furthermore, we found that increased integrin αβ heterodimerization resulted in monocyte/macrophage adhesion to endothelium. In conclusion, these results provided novel evidence that FFA-stimulated N--O stabilizes integrin βvia S-nitrosylation, favoring integrin αβ ligation to promote vascular inflammation.

Free fatty acids stabilize integrin βvia S-nitrosylation to promote monocyte-endothelial adhesion.

Psoriasis is a common chronic skin disorder. Pathologically, it features abnormal epidermal proliferation, infiltrating inflammatory cells and increased angiogenesis in the dermis. Aberrant expression of E3 ubiquitin ligase and a dysregulated protein ubiquitination system are implicated in the pathogenesis of psoriasis.

A critical role of the endothelial S-phase kinase-associated protein 2/phosphatase and tensin homologue axis in angiogenesis and psoriasis.

Drug-induced liver injury (DILI), especially acetaminophen overdose, is the leading cause of acute liver failure. Pregnane X receptor (PXR) is a nuclear receptor and the master regulator of drug metabolism. Aberrant activation of PXR plays a pathogenic role in the acetaminophen hepatotoxicity. Here, we aimed to examine the S-nitrosylation of PXR (SNO-PXR) in response to acetaminophen. We found that PXR was S-nitrosylated in hepatocytes and the mouse livers after exposure to acetaminophen or S-nitrosoglutathione (GSNO). Mass spectrometry and site-directed mutagenesis identified the cysteine 307 as the primary residue for S-nitrosylation (SNO) modification. In hepatocytes, SNO suppressed both agonist-induced (rifampicin and SR12813) and constitutively active PXR (VP-PXR, a human PXR fused to the minimal transactivator domain of the herpes virus transcription factor VP16) activations. Furthermore, in acetaminophen-overdosed mouse livers, PXR protein was decreased at the centrilobular regions overlapping with increased SNO. In PXR-/- mice, replenishing the livers with the SNO-deficient PXR significantly aggravated hepatic necrosis, increased HMGB1 release, and exacerbated liver injury and inflammation. Particularly, we demonstrated that S-nitrosoglutathione reductase (GSNOR) inhibitor N6022 promoted hepatoprotection by increasing the levels of SNO-PXR. In conclusion, PXR is posttranslationally modified by SNO in hepatocytes in response to acetaminophen. This modification mitigated the acetaminophen-induced PXR hyperactivity. It may serve as a target for therapeutical intervention.

S-nitrosylation attenuates pregnane X receptor hyperactivity and acetaminophen-induced liver injury.

Flow cytometry (FCM), characterized by its simplicity, rapid processing, multiparameter analysis, and high sensitivity, is widely used in the diagnosis, treatment, and prognosis of hematological malignancies. FCM testing of tissue samples not only aids in diagnosing and classifying hematological cancers, but also enables the detection of solid tumors. Its ability to detect numerous marker parameters from small samples is particularly useful when dealing with limited cell quantities, such as in fine-needle biopsy samples. This attribute not only addresses the challenge posed by small sample sizes, but also boosts the sensitivity of tumor cell detection. The significance of FCM in clinical and pathological applications continues to grow. To standardize the use of FCM in detecting hematological malignant cells in tissue samples and to improve quality control during the detection process, experts from the Cell Analysis Professional Committee of the Chinese Society of Biotechnology jointly drafted and agreed upon this consensus. This consensus was formulated based on current literature and clinical practices of all experts across clinical, laboratory, and pathological fields in China. It outlines a comprehensive workflow of FCM-based assay for the detection of hematological malignancies in tissue samples, including report content, interpretation, quality control, and key considerations. Additionally, it provides recommendations on antibody panel designs and analytical approaches to enhancing FCM tests, particularly in cases with limited sample sizes.

Chinese expert consensus on flow cytometric detection of hematological malignant cells in tissue samples.

Chromosomal karyotype analysis is crucial for diagnosing and managing hematologic malignancies, yet inconsistent protocols compromise reliability. To standardize practices, this consensus integrates international guidelines (WHO, ICC, ELN) with clinical expertise, providing evidence-based recommendations for specimen collection, cell culture, chromosome harvesting, banding techniques, karyotype analysis, and reporting. By establishing uniform operational standards, this initiative seeks to mitigate variability, improve detection rates, and support precision medicine in hematologic malignancies.

ArticleTotal : 2	Year
Publication title	2025
Publication title	2026

Article	Year
Evaluation of digital dental models obtained from dental cone-beam computed tomography scan of alginate impressions. Korean journal of orthodontics\| PubMed ID: 27226958	2016
Myeloid Cell mPges-1 Deletion Attenuates Mortality Without Affecting Remodeling After Acute Myocardial Infarction in Mice. The Journal of pharmacology and experimental therapeutics\| PubMed ID: 30992314	2019
[Research advances in relationship between biological clock and cardiovascular diseases]. Sheng li xue bao : [Acta physiologica Sinica]\| PubMed ID: 31646332	2019
Bmal1 Deletion in Myeloid Cells Attenuates Atherosclerotic Lesion Development and Restrains Abdominal Aortic Aneurysm Formation in Hyperlipidemic Mice. Arteriosclerosis, thrombosis, and vascular biology\| PubMed ID: 32321308	2020
Circadian Blood Pressure Rhythm in Cardiovascular and Renal Health and Disease. Biomolecules\| PubMed ID: 34207942	2021
Procyanidin B2 Attenuates Nicotine-Induced Hepatocyte Pyroptosis through a PPARγ-Dependent Mechanism. Nutrients\| PubMed ID: 35565726	2022
CCN1/Integrin αβ Instigates Free Fatty Acid-Induced Hepatocyte Lipid Accumulation and Pyroptosis through NLRP3 Inflammasome Activation. Nutrients\| PubMed ID: 36145246	2022
Free fatty acids stabilize integrin βvia S-nitrosylation to promote monocyte-endothelial adhesion. The Journal of biological chemistry\| PubMed ID: 36470423	2023
A critical role of the endothelial S-phase kinase-associated protein 2/phosphatase and tensin homologue axis in angiogenesis and psoriasis. The British journal of dermatology\| PubMed ID: 37850885	2024
S-nitrosylation attenuates pregnane X receptor hyperactivity and acetaminophen-induced liver injury. JCI insight\| PubMed ID: 38032737	2024
Chinese expert consensus on flow cytometric detection of hematological malignant cells in tissue samples. Journal of the National Cancer Center\| PubMed ID: 40040877	2025
Chinese expert consensus on hematologic malignancy karyotyping. Clinica chimica acta; international journal of clinical chemistry\| PubMed ID: 40721192	2026

Tingting Jiang

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