Date of Graduation

Summer 2017

Degree

Master of Science in Biology

Department

Biology

Committee Chair

Ryan Udan

Keywords

Vascular smooth muscle cells, vessel maturation, vascular development, angiogenesis, hemodynamic force

Subject Categories

Biophysics | Developmental Biology | Laboratory and Basic Science Research

Abstract

Throughout embryonic development, blood vessels are derived from endothelial cells by way of vasculogenesis. During angiogenesis, vessels remodel to form a hierarchy of large-diameter arteries that branch into small-diameter capillaries. In this maturation, vessels respond to unidentified signaling events to become surrounded with an outer layer of vascular smooth muscle cells (vSMCs). This results in arteries that have a thick vSMC layer, veins that have a thin vSMC layer, and capillaries that have a very thin or absent vSMC layer. What remains to be determined is the cause of the thicker layer of vSMCs around proximal arteries. Previous studies have implicated that mechanical forces provided by blood flow control the growth of arteries over capillaries. I hypothesize that these mechanical forces also determine the extent of vSMC coverage. To test this, I compared the extent of vSMC in arteries of normal-flow mouse embryos (wild type) with those in reduced-flow embryos (Myl7 [-/-] mutant). I observed less vSMC coverage in the proximal arteries from reduced-flow embryos versus normal-flow embryos. With immunostaining and confocal imaging, I determined that the amount of vSMCs did not differ between reduced-flow and normal-flow tissues. Reduced-flow tissues exhibit a failure of the vSMCs to migrate away from capillaries towards proximal arteries, and a failure to surround the arteries. My findings provide evidence that hemodynamic force is required for vSMC recruitment, but not for vSMC differentiation or proliferation.

Copyright

© Rachel Lee Padget

Open Access

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