David WeberAssociate Professor
Department of Physiology,
University of South Alabama
College of Medicine

E-mail: dweber@southalabama.edu

Mailing address:
Department of Physiology
5851 USA Dr. N., MSB 3074
University of South Alabama
Mobile, Alabama 36688

Ph.D., Physiology, Medical College of Wisconsin.
Postdoctoral Studies: Division of Cardiology, Emory University, Georgia.  Department of Physiology, Medical College of Georgia and University of Michigan Medical School.

Research Interests:  

Oxidative stress, defined as an increase in reactive oxygen species (ROS) in the vasculature, has been implicated in several pathologic conditions affecting the cardiovascular system including hypertension, athlerosclerosis, and restenosis following balloon injury. Each of these conditions is associated with significant vascular damage and repair. Adjacent normal tissue facilitates the repair process and formation of neointima by both proliferation and migration. Several growth factors, including the potent platelet-derived growth factor (PDGF), stimulate vascular smooth muscle cell (VSMC) migration from the media to the neointima. Exposure of vascular smooth muscle cells to PDGF also results in generation of ROS, and ROS have been shown to have significant effects on both the growth and migration of vascular smooth muscle cells.

Therefore, the focus of my current studies is to test the hypothesis that ROS are critical mediators of VSMC migration. Two specific aims are being addressed; 1) to define signaling steps that mediate PDGF-induced VSMC migration and determine which are ROS sensitive, and 2) to define the contribution of ROS in vivo by studying migration and remodeling during restenosis following vascular injury in transgenic mice producing altered levels of ROS. These studies utilize several techniques including 1) the use of transwell migration assays using cultured VSMC following pharmacological interventions to examine mediators of migration, 2) immunoblotting, immunoprecipitation, and activity assays in cultured VSMC following pharmacological intervention or adenoviral infection to determine the redox-sensitivity of signaling mechanisms associated with migration, and 3) the use of transgenic mice that have VSMC-specific alterations in ROS levels to study the redox-sensitivity of signaling mechanisms during the process of restenosis induced by wire injury of the femoral artery.

Recent Publications:

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