2013 OSU Molecular Life Sciences
Interdisciplinary Graduate Programs Symposium
Poster abstracts
Abstract:
Mature vascular smooth muscle cells (VSMCs) have phenotypic plasticity that allows them to transition between contractile, proliferative and synthetic phenotypes in response to environmental cues or blood vessel injury. A primary focus of our lab has been to understand the signaling interactions between endothelial cells and vascular smooth muscle cells. In this current study, we sought to explore how signaling between endothelial cells and VSMCs influenced VSMC phenotypic switching. Previous studies from our lab indicated that endothelial cells induce smooth muscle specific gene expression when cocultured with smooth muscle cells or their precursors, mesenchymal stem cells (MSCs). Interestingly, our results have shown that endothelial cells not only induce a contractile phenotype in SMCs and MSCs, but also repress cell proliferation. Furthermore, our data indicate that cocultured endothelial cells can induce a synthetic phenotype as measured by collagen synthesis, suggesting that endothelial cells can modulate phenotypic switching. Our findings have further demonstrated that endothelial cell-induced Notch signaling plays a critical role in the regulation of SMC differentiation and phenotypic modulation. These studies are poised to elucidate the regulatory role that endothelial cell signaling has on smooth muscle cell phenotypes. A better knowledge of how endothelial cells regulate SMC phenotypic properties will facilitate the development of innovative treatments to improve cardiovascular disease outcomes.
Keywords: Notch , SMC phenotypic modulation