Corin protects H₂O₂-induced apoptosis through PI3K/AKT and NF-κB pathway in cardiomyocytes

Area of Science:

• Cardiovascular Biology
• Cellular Stress Response
• Molecular Cardiology

Background:

• The role of corin in hydrogen peroxide (H₂O₂)-induced apoptosis in cardiomyocytes remains largely uncharacterized.
• This study investigates corin's protective effects against H₂O₂-induced cardiomyocyte injury.
• Potential involvement of PI3K/AKT and NF-kB signaling pathways in corin's protective mechanism is explored.

Purpose of the Study:

• To elucidate the protective function of corin against H₂O₂-induced cellular damage in cardiomyocytes.
• To determine the involvement of PI3K/AKT and NF-kB signaling pathways in corin-mediated cardioprotection.
• To investigate the effect of corin on reactive oxygen species (ROS) levels and HIF-1α expression.

Main Methods:

• Utilized H9c2 and HL-1 cardiomyocyte cell lines.
• Assessed cell viability (CCK-8), apoptosis (flow cytometry, TUNEL, Western blot), and migration (wound healing assay).
• Measured reactive oxygen species (ROS) levels, and corin, apoptosis-related proteins, and signaling pathway protein expression (qRT-PCR, Western blot).

Main Results:

• H₂O₂ treatment reduced cell viability and migration, increased apoptosis, and decreased corin expression in cardiomyocytes.
• Corin overexpression counteracted H₂O₂-induced injury, enhancing cell viability and migration while reducing apoptosis.
• Corin overexpression decreased ROS levels, potentially via HIF-1α upregulation, and activated PI3K/AKT and NF-kB pathways.

Conclusions:

• Corin confers significant protection to cardiomyocytes against H₂O₂-induced injury.
• Corin's protective effects are mediated by the downregulation of apoptosis and ROS levels.
• Activation of PI3K/AKT and NF-kB signaling pathways, along with HIF-1α upregulation, are key mechanisms in corin's cardioprotection.