Deletion of SM22α disrupts the structure and function of caveolae and T-tubules in cardiomyocytes, contributing to heart failure.

ABSTRACT:

Aims

Smooth muscle 22-alpha (SM22α) is an actin-binding protein that plays critical roles in mediating polymerization of actin filaments and stretch sensitivity of cytoskeleton in vascular smooth muscle cells (VSMCs). Multiple lines of evidence indicate the existence of SM22α in cardiomyocytes. Here, we investigated the effect of cardiac SM22α on the membrane architecture and functions of cardiomyocytes to pressure overload.

Methods

SM22α knock-out (KO) mice were utilized to assess the role of SM22α in the heart. Echocardiography was used to evaluate cardiac function, transverse aortic constriction (TAC) was used to induce heart failure, cell shortening properties were measured by IonOptix devices in intact cardiomyocytes, Ca2+ sensitivity of myofilaments was measured in per

SUBMITTER: Wu J 

PROVIDER: S-EPMC9292107 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature