Date of Award

12-2011

Degree Name

MS in Biomedical Engineering

Department/Program

Biomedical and General Engineering

Advisor

Trevor Cardinal

Abstract

Peripheral Artery Disease is a very serious disease characterized by an arterial occlusion due to atherosclerotic plaques. In response to an arterial occlusion, arteriogenesis occurs, causing smooth muscle cells to transition from a contractile to synthetic state. Also following an arterial occlusion, functional impairment was seen in the collateral circuit. An immunofluorescence protocol was developed in order to assess the impact of collateral enlargement (arteriogenesis) on smooth muscle phenotype at various time points. Smooth muscle α-actin was used to mark all smooth muscle cells, Ki-67 was used to label proliferating smooth muscle cells, and a fluorescent nuclear stain was used to quantify the number of cells present. Samples of the profunda femoris and gracilis were dissected from each mouse hind limb (one ligated, one sham) at three different time points: 3 days, 7 days, and 14 days after a femoral artery ligation surgery. Smooth muscle cell phenotype and luminal cross-sectional area were assessed in the profunda femoris and the midzone of the gracilis collaterals. Smooth muscle cells were proliferating at 3 and 7 days following the occlusion in the gracilis collaterals and significant collateral vessel growth was observed over the two week period. No proliferation was observed in the profunda femoris and although there was an increasing trend in vessel size over the two week period, the averages were not significantly different. The phenotypic transition of the smooth muscle cells was not the cause of vascular impairment in the collateral circuit. This shows that further research is needed to characterize impairment in the collateral circuit.

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