Lead-induced cardiomyocytes apoptosis by inhibiting gap junction intercellular communication via autophagy activation

Lead (Pb) is one of the most common heavy metal contaminants in environment. Pb can cause pathophysiological changes several organ systems, including cardiovascular system, but molecular mechanism remains elusive. The study aimed to effects on Gap junction intercellular communication (GJIC) and its role Pb-induced apoptosis. present aims determine whether autophagy promotes apoptosis rat cardiac myocytes (H9c2 cells) by downregulating GJIC using CCK-8 Kit, scrape loading/dye transfer assay, Annexin V/PI assays, Western blot analysis double-immunofluorescence experiments. results showed that elicited cytotoxicity a time- concentration-dependent manner led increased H9c2 cells. also reduced cells through downregulation connexin (Cx) 43. Inhibition gap junctions blocker carbenoxolone disodium (CBX) resulted Furthermore, cells, decreasing distribution Cx43 cell membrane, targeted autophagosome via light chain 3 (LC3). However, inhibitor 3-Methyladenine (3-MA) slow down induced In conclusion, our provide evidence Pb-decreased cardiomyocytes. This probably because fact exacerbates inhibition Cx43.