下调和上调
连环素
细胞凋亡
程序性细胞死亡
活力测定
医学
癌症研究
细胞
Wnt信号通路
连环蛋白
细胞生物学
内科学
化学
信号转导
生物
生物化学
基因
作者
Haofei Kang,Weiwei Jiang
出处
期刊:Clinics
[Fundacao Faculdade de Medicina]
日期:2023-01-01
卷期号:78: 100189-100189
标识
DOI:10.1016/j.clinsp.2023.100189
摘要
To explore whether the effect of β-catenin on MI and MI-induced cardiomyocyte apoptosis is YAP-dependent.The authors established an MI rat model by ligating the anterior descending branch of the left coronary artery, and an MI cell model by treating cardiomyocytes with H2O2.β-catenin downregulation was observed in MI cardiac tissues and in H2O2-treated cardiomyocytes. Lentiviral-CTNNB1 was administered to MI rats to upregulate β-catenin expression in MI cardiac tissue. β-catenin recovery reduced the myocardial infarct area, fibrosis, and apoptotic cell death in MI rats. H2O2 treatment attenuated cell viability and induced cell death in cardiomyocytes, whereas β-catenin overexpression partially reversed these changes. Moreover, H2O2 treatment caused the deactivation of Yes-Associated Protein (YAP), as detected by increased YAP phosphorylation and reduced the nuclear localization of YAP. Upregulation of β-catenin expression reactivated YAP in H2O2-treated cardiomyocytes. Reactivation of YAP was achieved by administration of Mitochonic Acid-5 (MA-5) to H2O2-treated cardiomyocytes, and deactivation of YAP by CIL56 treatment in β-catenin-overexpressing H2O2-treated cardiomyocytes. MA-5 administration increased cell viability and repressed apoptosis in H2O2-treated cardiomyocytes, whereas CIL56 treatment counteracted the effects of β-catenin overexpression on cell survival and apoptosis.The present data indicate that β-catenin and YAP are effective treatment targets for MI, blocking the apoptotic death of cardiomyocytes.
科研通智能强力驱动
Strongly Powered by AbleSci AI