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Your search keyword '"Pan, Jianyuan"' showing total 5 results
Start Over Author "Pan, Jianyuan" Publisher lippincott williams & wilkins
5 results on '"Pan, Jianyuan"'

3. Higher serum level of Cystatin C

Author

Chen, Zhenfei, Zhang, Jing, Feng, Jun, Zhou, Gaoliang, Jin, Xiaoqin, and Pan, Jianyuan

Subjects
Adult, Male, Gensini score, Observational Study, Coronary Artery Disease, urologic and male genital diseases, Risk Assessment, cystatin C, Humans, Homocysteine, Triglycerides, Aged, Aged, 80 and over, coronary artery lesions, Middle Aged, Uric Acid, Lipoproteins, LDL, Cholesterol, Logistic Models, Heart Disease Risk Factors, Female, Lipoproteins, HDL, Biomarkers, Research Article, Glomerular Filtration Rate
Abstract

Cystatin C has been proposed as a useful biomarker of early impaired kidney function and a predictor of mortality risk. The present study is to investigate the association between serum Cystatin C and the severity of coronary artery lesions, Gensini score (GS), and the risk of coronary artery disease (CAD). A total of 682 CAD patients (230 females, 452 males; mean age 62.6 ± 10.7 years, range from 31 to 86 years) and 135 controls (41 females, 94 males; mean age 58.0 ± 10.3 years, range from 38 to 84 years) were recruited in the present study. Enzyme-linked immunosorbent assay was applied to measure serum cystatin C levels and other serum indexes. The estimated glomerular filtration rate and GS were calculated. Serum low-density lipoprotein cholesterol (LDL-C), uric acid, Cystatin C, and homocysteine (HCY) were significantly elevated in CAD patients compared to controls. There were significant differences regarding total cholesterol, triglyceride, high-density lipoprotein, low-density lipoprotein, cystatin C, eGFR and GS among stable angina pectoris (SAP), unstable angina group (UAP), and acute myocardial infarction (AMI) patients. AMI group had an elevated serum Cystatin C, LDL-C, HCY, and GS than SAP and UAP patients. When stratified patient groups by the quartiles of Cystatin C, we found age, the proportion of male and patients with diabetes, HCY, and GS were increased in Q4 than in other quartile groups. Spearman correlation test revealed a positive relationship between Cystatin C, HCY, and GS. Multivariate logistic regression analysis revealed that serum Cystatin C level, presence of hypertension and diabetes, HCY, age, and male were the risk factors for coronary artery lesions. In summary, our results suggested that cystatin C is a promising clinical biomarker that provides complementary information to the established risk determinants. The serum Cystatin C level is strongly associated with GS and could be used to evaluate the severity of coronary artery lesions.

Published
2021

5. Upregulating MicroRNA-203 Alleviates Myocardial Remodeling and Cell Apoptosis Through Downregulating Protein Tyrosine Phosphatase 1B in Rats With Myocardial Infarction.

Author

Zhang J, Pan J, Yang M, Jin X, Feng J, Wang A, and Chen Z

Subjects
Animals, Apoptosis Regulatory Proteins metabolism, Cell Hypoxia, Cell Line, Disease Models, Animal, MicroRNAs genetics, Mitochondria, Heart pathology, Myocardial Infarction genetics, Myocardial Infarction pathology, Myocardial Infarction physiopathology, Myocytes, Cardiac pathology, Protein Tyrosine Phosphatase, Non-Receptor Type 1 genetics, Rats, Sprague-Dawley, Signal Transduction, Up-Regulation, Apoptosis, MicroRNAs metabolism, Mitochondria, Heart enzymology, Myocardial Infarction enzymology, Myocytes, Cardiac enzymology, Protein Tyrosine Phosphatase, Non-Receptor Type 1 metabolism, Ventricular Function, Left, Ventricular Remodeling
Abstract

Myocardial infarction (MI) is one of cardiovascular diseases with high incidence and mortality. MicroRNAs, as posttranscriptional regulators of genes, are involved in many diseases, including cardiovascular diseases. The aim of the present study was to determine whether miR-203 was functional in MI therapy and how it worked. Left anterior descending artery ligation and hypoxia/reoxygenation (H/R) treatment were, respectively, performed to obtain MI rats and hypoxia-injured H9c2 cells. Western blot and quantitative real-time polymerase chain reaction were used to determine protein levels and messenger RNA of relevant genes, respectively. Lentivirus-mediated overexpression of miR-203 was performed to study the miR-203 functions on left ventricular remodeling, infarct size, and cardiomyocyte apoptosis. Compared with the sham group, miR-203 levels were significantly decreased in MI and H/R groups. However, overexpressing miR-203 greatly improved the cardiac function, reduced infarct size in rats after MI and weakened infarction-induced apoptosis by increasing Bcl-2 and reducing decreasing Bax, cleaved caspase-3, and cleaved caspase-9. In addition, Protein tyrosine phosphatase 1B (PTP1B) was proved as a target of miR-203 in cardiomyocytes, and it was negatively regulated by miR-203. Further experiments indicated that PTP1B overexpression could remarkably inhibit miR-203-mediated antiapoptosis of cardiomyocytes and alleviate protective effects of miR-203 on mitochondria after H/R treatment. Altogether, miR-203 prevented infarction-induced apoptosis by regulating PTP1B, including reducing proapoptosis proteins, inactivating caspase pathway, and protecting mitochondria. In conclusion, miR-203 had abilities to alleviate MI-caused injury on myocardium tissues and reduce mitochondria-mediated apoptosis, which might be a potential target used for MI therapy.

Published
2019
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