Apelin-13 regulates angiotensin II-induced Cx43 downregulation and autophagy via the AMPK/mTOR signaling pathway in HL-1 cells

Title:

Apelin-13 regulates angiotensin II-induced Cx43 downregulation and autophagy via the AMPK/mTOR signaling pathway in HL-1 cells

Creator:

Chen, Yifan, Qiao, Xi, Zhang, Lijun, Li, Xuewen, and Liu, Qinghua

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f312b432-9435-4624-9cb5-3d640035514e
uuid:f312b432-9435-4624-9cb5-3d640035514e
issn:0862-8408
doi:10.33549/physiolres.934488

Subject:

fibrilace síní, atrial fibrillation, Cx43, cell hypertrophy, AMPK/mTOR, autophagy, 14, and 612

Type:

model:article and TEXT

Format:

počítač and online zdroj

Description:

Atrial fibrillation is associated with atrial remodeling, in which connexin 43 (Cx43) and cell hypertrophy play important roles. In this study, apelin-13, an aliphatic peptide, was used to explore the protective effects of the adenosine monophosphate-activated protein kinase (AMPK)/mTOR signaling pathway on Cx43 expression and autophagy, using murine atrial HL-1 cells. The expression of Cx43, AMPK, B-type natriuretic peptide (BNP) and pathway-related proteins was detected by Western blot analysis. Cellular fluorescence imaging was used to visualize Cx43 distribution and the cytoskeleton. Our results showed that the Cx43 expression was significantly decreased in HL-1 cells treated with angiotensin II but increased in cells additionally treated with apelin-13. Meanwhile, apelin-13 decreased BNP expression and increased AMPK expression. However, the expression of Cx43 and LC3 increased by apelin-13 was inhibited by treatment with compound C, an AMPK inhibitor. In addition, rapamycin, an mTOR inhibitor, promoted the development of autophagy, further inhibited the protective effect on Cx43 expression and increased cell hypertrophy. Thus, apelin-13 enhances Cx43 expression and autophagy via the AMPK/mTOR signaling pathway, and serving as a potential therapeutic target for atrial fibrillation., Yifan Chen, Xi Qiao, Lijun Zhang, Xuewen Li, Qinghua Liu., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Coverage:

813-822

Source:

Physiological research | 2020 Volume:69 | Number:5

Harvested from:

CDK

Metadata only:

false