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Current Projects and Interests: Mechanisms of Complement-induced Injury — We have shown that complement is activated immediately upon reperfusion of the ischemic myocardium. Administration of murine anti-porcine C5a or anti-rat C5 monoclonal antibody (MoAb) attenuates reperfusion induced myocardial injury. Current studies investigate the mechanisms involved in this protection (i.e., decreased PMN activation/adherence, preservation of endothelial cell integrity, etc.). Complement and Endothelial Dysfunction — The effects of complement on the vascular endothelium are not well characterized. We have shown that complement activation directly attenuates endothelium-dependent relaxation of vascular smooth muscle. Further, C5 plays an important role in the upregulation of adherence molecules via NF-kB translocation and cGMP mechanisms. We are investigating the effects of oxidative stress on complement activation in vitro and in vivo.
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