Poster Session 1 - C7
1,2Sarah K. Steinbach, 1,7,10Tao Wang, 1Martha H. Carruthers, 2,4,5,9Angela Li, 2,4,5,8Rickvinder Besla, 11Adam P. Johnston, 2,4,5,8,9Clinton S. Robbins, 1,3-8,10Mansoor Husain
1 Division of Experimental Therapeutics, Toronto General Hospital Research Institute, University Health Network; 2 Division of Advanced Diagnostics, Toronto General Hospital Research Institute, University Health Network; 3 McEwen Centre for Regenerative Medicine; 4 Ted Rogers Centre for Heart Research; 5 Peter Munk Cardiac Centre, University Health Network; 6 Department of Medicine, University of Toronto; 7 Department of Physiology, University of Toronto; 8 Department of Laboratory Medicine & Pathobiology, University of Toronto; 9 Department of Immunology, University of Toronto; 10 Cardiovascular Sciences Collaborative Program, University of Toronto; 11 Hospital for Sick Children
Vascular smooth muscle cells (VSMC) in the mouse aorta significantly contribute to cardiovascular health and disease and are derived from distinct embryological lineages. Aortic Sca-1+ vascular smooth muscle progenitor cells give rise to VSMC; however, the developmental origins of these progenitors, and the specific role of the VSMC derived from them, are unknown. Lineage tracing of Myf5-expressing embryological tissues (i.e. somitic mesoderm) following tamoxifen-induced recombination at E8.5 reveals that 45±6% of aortic Sca-1+ cells in adult mice arise from the somitic mesoderm. These somite-derived Sca-1+ cells expand between 4-6 weeks after birth and become a major contributor to the adult mouse aorta. This expansion occurs independent of bone marrow, spleen, blood, or circulating cells. What requires further investigation are the role of these Sca-1+ VSMC progenitors in diseases such as hypertension or aortic aneurysm, and the significance of post-natal aortic Sca-1+ cell expansion. We note somite-derived Sca-1+ VSMC progenitors as a distinct population of Sca-1+ progenitors, but whether differences exist between somite-derived Sca-1+ VSMC progenitors and other VSMC progenitors remains unexplored. We posit that a better understanding of the contributions of VSMC progenitors may reveal their roles in vascular diseases which may rationalize their therapeutic targeting.