Endothelial HSPA12B Exerts Protection Against Sepsis-Induced Severe Cardiomyopathy via Suppression of Adhesion Molecule Expression by miR-126.

ABSTRACT: Heat shock protein A12B (HSPA12B) is predominately expressed in endothelial cells (ECs) and has been reported to protect against cardiac dysfunction from endotoxemia or myocardial infarction. This study investigated the mechanisms by which endothelial HSPA12B protects polymicrobial sepsis-induced cardiomyopathy. Wild-type (WT) and endothelial HSPA12B knockout (HSPA12B^-/-) mice were subjected to polymicrobial sepsis induced by cecal ligation and puncture (CLP). Cecal ligation and puncture sepsis accelerated mortality and caused severe cardiac dysfunction in HSPA12B^-/- mice compared with WT septic mice. The levels of adhesion molecules and the infiltrated immune cells in the myocardium of HSPA12B^-/- septic mice were markedly greater than in WT septic mice. Th

SUBMITTER: Zhang X 

PROVIDER: S-EPMC7201039 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature