The Use of p66Shc Knockout Mice to Investigate the Mechanisms Responsible for Cardiomyocyte Apoptosis With AgePI: Leeuwenburgh, Christiaan, PhD
Funding Agency: American Heart Association
Agency Project Number: 0415166B
Start Date: Jul 1, 2004
End Date: Jun 30, 2006
We hypothesize that the p66Shc deficient mice will have a diminished basal mitochondrial oxidant generation, and oxidative damage with age, compared to littermate controls, and an attenuated cardiomyocyte apoptosis. We will evaluate mitochondrial function by measuring key components of the mitochondrial oxidative stress markers. Moreover, we will quantify apoptosis and levels of specific pro- and anti-apoptotic proteins, markers and inhibitors of apoptosis. The proposed study will improve our understanding of the cellular mechanisms involved in myocyte loss with aging, and is a critical step toward the development of specific therapeutic interventions that can attenuate this cell loss and possibly reduce the incidence of cardiovascular disease.
Christiaan Leeuwenburgh, Ph.D. Asimina Hiona, M.S.