Loading…
GW29-e1603 The effect of activin A-follistatin system imbalance on myocardial fibrosis of heart failure and the regulation of ghrelin
[...]the purpose of this study is to elucidated the effect of the imbalance of Act A-FS system on the progression of heart failure, and whether ghrelin can prevent heart failure by regulating the imbalance of Act A-FS system.Methods In the study, the left anterior descending coronary artery was liga...
Saved in:
Published in: | Journal of the American College of Cardiology 2018-10, Vol.72 (16), p.C49-C49 |
---|---|
Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | [...]the purpose of this study is to elucidated the effect of the imbalance of Act A-FS system on the progression of heart failure, and whether ghrelin can prevent heart failure by regulating the imbalance of Act A-FS system.Methods In the study, the left anterior descending coronary artery was ligated to establish a rat model of heart failure (HF), and then treated with ghrelin (100 μg/kg, subcutaneous injection, bid); the cardiomyocytes from neonatal rats were cultured and stimulated with Ang II (0.1 μM) and ghrelin (0.1 μM) to explore the role and mechanism of ghrelin in myocardial remodeling. To further explore whether ghrelin inhibits myocardial fibrosis by improving Act A-FS system imbalance, the levels of Act A and FS were examined by immunohistochemistry, real-time quantitative PCR and ELISA in vivo and in vitro; Finally, to investigate the effect of overexpressed Act A on myocardial fibrosis, the primary rat cardiac fibroblasts (CFs) were cultured and treated with Act A, the proliferation of CFs was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Furthermore, ghrelin decreased Ang II-induced Act A expression with no effect on FS expression in primary rat cardiomyocytes in vitro. [...]ghrelin corrected the Act A /FS imbalance. |
---|---|
ISSN: | 0735-1097 1558-3597 |
DOI: | 10.1016/j.jacc.2018.08.182 |