BIN1 Isoform 1 has Less Function in Promoting the Stability of TAT System in Adult Rat Cardiomyocytes

Abstract

The process of heart electrical excitation to contraction is called excitation-contraction coupling, which is important for heart to propel blood out. Transverse-axial-tubule (TAT) system in Ventricular myocyte, including classic transverse tubules (TTs) and axial tubules (ATs), is complex tubular structure formed by invaginations of sarcolemma. During many heart diseases, such as arrhythmia, hypertrophy and heart failure, TAT system become disordered which affecting the efficiency of E-C coupling. In heart cell, membrane shape regulation is important for many cellular functions. According to literature report Bin/Amphyiphysin/Rvs (BAR) domain-containing proteins play important role in membrane remodeling during the basic cell life activities such as endocytosis, cell migration, and endosomal sorting. In striated muscle, BIN1 is assumed to be very important palyer in inducing cytomembrane invagination to form the TAT system. BIN1 mutations and misregulation of splicing cause diseases in skeletal muscle and brain, and cardiac isoform of BIN1 (BIN1+13+17 or cBIN1) is known to organize cardiac TT microdomains, but the role of other BIN1 isoforms in heart remains elusive. We are curious about the role of BIN1 isoform 1 and whether it can maintain or promote TAT system stability in cultured adult myocytes. So we transfected adult rat cardiomyocytes with adenovirus of DsRed-BIN1 isoform 1. The results showed that overexpression of BIN1 isoform 1 didn't show a significant positive effect on maintaining or promoting the stability of TAT system in adult cardiomyocytes