Abstract 236: Vascular Smooth Muscle Cells Stimulate Re-endothelialization Through Protein Kinase C-delta-dependent Release Of CXCL7 and Recruitment of Circulating Angiogenic Cells

Objective: In response of injury, vascular smooth muscle cells (VSMCs) undergo proliferation, migration, as well as apoptosis. We have previously shown that gene transfer of a pro-apoptotic mediator protein kinase C-delta (PKCδ) reduces intimal hyperplasia. Subsequently, we showed that VSMCs are a rich source of chemokines. In this study, we explored whether VSMCs may play a role in regulation of re-endothelialization through PKCδ-dependent release of chemokines. Methods and Results: We constructed an adenovirus that expresses PKCδ under VSMC-specific SM22 promoter (AdPKCδ) and use it to drive PKCδ expression in VSMCs of injured rat carotid arteries. Compared to the empty vector (AdNull), AdPKCδ accelerated re-endothelialization, reflected by a larger area that was excluded of Evan’s blue (25.38±7.52% v.s 59.60±5.01%). Media conditioned by PKCδhigh VSMCs had no measurable effects on endothelial cell functions, including BrdU incorporation, transwell migration, scratch wound healing, and tube formation. In...