A role of AMPK and connexin 43 in the suppression of CoCl 2 -induced apoptosis of spiral modiolar artery smooth muscle cells by adiponectin.

Aims: Adiponectin (APN) is a protein hormone secreted mainly by adipose tissue that exhibits biological functions such as anti-inflammatory, anti-atherosclerotic, anti-apoptotic, hearing-protective and microcirculation-regulating functions. In this study, we explored whether APN could attenuate damage caused by CoCl ₂ -induced hypoxic conditions in smooth muscle cells (SMCs) of the spiral modiolar artery (SMA).
Main Methods: We first cultured and identified primary SMCs of the SMA. Afterward, the SMCs were pre-treated with APN and then stimulated with CoCl ₂ .
Key Findings: Compared with the control group, the group treated with CoCl ₂ for 24 h exhibited significantly decreased cell viability, significantly increased apoptosis rates and Malondialdehyde (MDA) levels, and decreased Superoxide Dismutase (SOD) activity. In addition, the expression levels of Bax and cleaved caspase-3 were upregulated, while those of Bcl2 were downregulated evidently. Compared with the CoCl ₂ group, the group pre-treated with APN before receiving CoCl ₂ treatment had increased cell viability and SOD activity but decreased MDA levels and apoptosis rates. The expression levels of Bcl2, p-AMPKα and Cx43 were evidently increased, while those of Bax and cleaved caspase-3 were decreased, in the group pre-treated with APN compared to the CoCl ₂ group. The protective effect of APN was blocked by the AMPK inhibitor Compound C and the Cx43 inhibitor Gap19.
Significance: Our study demonstrated that APN protected SMCs against CoCl ₂ -induced hypoxic injury via the AMPK signalling pathway and regulated the expression of Cx43 in cells. Therefore, APN might be a promising treatment for diseases related to circulation disturbances of the inner ear.
(Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)