Skeletal myoblasts and bone marrow cells enhance contractility of failing cardiomyocytes in co-culture

Abstract

Cell transplantation has been shown to enhance ventricular function in heart failure, but the mechanisms responsible remain unknown. We hypothesized that bone marrow mononuclear cells and skeletal myoblasts cells can influence cardiomyocytes by paracrine mechanisms. Myocardial infarction was induced in adult female Sprague–Dawley rats. Left ventricular ejection fraction after 3 weeks was 35.5±2.0%. Isolated failing left ventricular myocytes were cultured (density 5.2 cells/mm2) on their own (Control) or with either bone marrow mononuclear cells (BM, density 52 cells/mm2) or skeletal myoblasts (SK, density 5.2 cells/mm2). BM and SK were separated from the failing cardiomyocytes by a Transwell™ porous membrane. After 48 h of co-culture with SK or BM cardiomyocyte relaxation speed was increased. The decay time course of the indo-1 transient was also hastened by SK. SK, but not BM, also increased the cardiomyocyte contraction amplitude compared to Control. Tabled 1 Control BM SK Sarcomere shortening (nm) 46±6 55±1 91±14* Sarcomere relaxation T50 (ms) 34±6 18±3* 13±2* Indo-1 decay T50 (ms) 22±2 18±2 13±1* (Data represented as mean±SEM, *p<0.05 vs. Control) Open table in a new tab