Corin protects H2O2-induced apoptosis through PI3K/AKT and NF-κB pathway in cardiomyocytes - 31/12/17
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Abstract |
Background |
The functional role of corin in H2O2-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.
Method |
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.
Results |
Treatment with H2O2 (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 H2O2-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.
Conclusion |
Overexpression of corin protected cardiomyocytes from H2O2-induced injury by decreasing apoptosis and ROS level via activations of the PI3K/AKT and NF-κB signaling pathways and upregulating HIF-1α.
Le texte complet de cet article est disponible en PDF.Keywords : Corin, Cardiomyocytes, Cell injury, PI3K/AKT pathway, NF-κB pathway
Plan
Vol 97
P. 594-599 - janvier 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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