Heart muscle development

Cardiomyocytes (CM) in vertebrates lack a significant regenerative potential, as these cells withdraw from cell cycle shortly after birth. However, it was recently shown that CM in zebrafish and neonate mammals can regenerate an injured heart. The specific mechanisms responsible for this residual proliferative potential are, however, unclear. In this study, we explore the possibility that the mechanical properties of the CM microenvironment, specifically, substrate rigidity, affect CM differentiation and proliferation. Our results demonstrate that CMs grown on different rigidities present different proliferative capacity, as well as morphological changes, suggesting an essential role for the microenvironment in CM cell-cycle control (Figure 1).

Figure 11

Cardiomyocyte cell-cycle control. 1-day old rat cardiomyocyte cultured on rigid substrate (2MPa), immunostained for cardiac troponin T (cTnT, green), proliferation marker Ki67 (red), and DAPI (blue).

In collaboration with Prof. Eldad Tzahor, Department of Biological Regulation at the Weizmann Institute.