Exosome-Derived Mirnas Mediate Cardiomyocyte-Adipocyte Communication And Suppress High Molecule Adiponectin Production By Regulating Er Function After Myocardial Ischemia/Reperfusion

Despite years of significant effort, it remains unclear how injured cardiomyocytes disrupt gene synthesis in adipocytes. We recently demonstrate cardiac ischemia/reperfusion (I/R) injury markedly releases exosomes. In our current discovery-based study, we determined the specific effect of cardiac-derived exosomes upon gene expression. By investigating genes regulating various cellular processes (including inflammation, lipid biosynthesis, lipolysis, glycometabolism, β oxidation, adipokine, apoptosis and ER stress), we demonstrate that cardiac-derived exosomes upregulated 1 cytokine and 5 ER stress genes (CHOP, Gadd34), and decreased the expression of 2 ER stress genes (EDEM1, DERL1) in adipose tissue in vivo. To further investigate the dysregulation of ER stress, ERp44 and DsBA-L1 was measured. Cardiac I/R-derived exosomes suppressed expression of both ERp44 and DsBA-L1 in vitro and in vivo, supporting the role of exosome-induced ER stress in target cells. In 3T3L1 cells subjected to cardiac I/R-derived e...