Caco-2 cells labeled for tight junction molecule cingulin (green), actin (red), vinculin (pink) and DNA (blue).
Epithelial cells growing on a patterned adhesive surface with the shape of the Weizmann Institute tree.
Desmosomes in mouse tongue epithelium (by transmission electron microscope).
Porcine aortic endothelial cell, double-labeled for actin (green) and phospho-tyrosine (red).
“Molecular composition map” of focal adhesions and stress fibers.
Myeloma cancer cell responding to shear flow (by scanning electron microscope).
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.