Corin protects H 2 O 2 -induced apoptosis through PI3K/AKT and NF-κB pathway in cardiomyocytes

• Published in: Biomedicine & pharmacotherapy Vol. 97; p. 594
• Main Authors: Li, Yansong, Xia, Jingwen, Jiang, Nianxin, Xian, Yuqiong, Ju, Haining, Wei, Yong, Zhang, Xuan
• Format: Journal Article
• Language: English
• Published: France 01.01.2018
• Subjects: Cell injury; NF-κB pathway; Cardiomyocytes; Corin; PI3K/AKT pathway
• ISSN: 1950-6007

The functional role of corin in H O -induced apoptosis is largely unexplored. The present study investigated the protective role of corin against cell injury by possible involvement of PI3K/AKT and NF-kB signaling pathways in cardiomyocytes. Cardiomyocytes H9c2 and HL-1 cells were used in the study. Cell viability was measured using CCK-8 assay; cell apoptosis was analyzed by flow cytometry, TUNEL assay, and western blot; and cell migration was measured using wound healing assay. The fluorescent intensities of reactive oxygen species (ROS) were measured using a flow cytometer. Quantitative RT-PCR was used to measure the mRNA expression of corin. Western blot was used to measure the protein expression of corin, apoptosis-related proteins (Bax, cleaved-Caspase-3 and -9), and PI3K/AKT and NF-κB signaling pathway proteins. Treatment with H O (150μM, 6h) significantly decreased cell viability and relative migration, increased apoptosis, and decreased the expression of corin in H9c2 and HL-1 cells. Overexpression of corin alleviated the H O -induced cell injury by increasing cell viability and migration and decreasing apoptosis in the cardiomyocytes. Overexpression of corin also decreased the ROS level in the cardiomyocytes likely through upregulating HIF-1α. These effects of corin on the cell injury might be mediated via the corin-induced activations of PI3K/AKT and NF-κB signaling pathways. Overexpression of corin protected cardiomyocytes from H O -induced injury by decreasing apoptosis and ROS level via activations of the PI3K/AKT and NF-κB signaling pathways and upregulating HIF-1α.