Date of Award
2006
Degree Type
Thesis
Degree Name
Master of Science
Program
Pathology
Supervisor
Dr. Subrata Chakrabarti
Second Advisor
Dr. George Cherian
Third Advisor
Dr. Rennian Wang
Abstract
Oxidative stress is involved in the pathogenesis of diabetic cardiomyopathy. The localization of CD36 and endothelial nitric oxide synthase (eNOS) to the cell membrane caveolea may provide a model for the ∞ntinuous production of oxidative stress in diabetes. We hypothesized that hyperglycemia may lead to increased oxidative stress and reduced nitric oxide bioavailability through the alteration of CD36∕eNOS axis. Analysis of the heart tissues from diabetic animals revealed transcriptional upregulation of CD36 and eNOS. These changes were associated with increased oxidative damage. Microvascular endothelial cells (MVECs) exposed to high levels of glu∞se increase CD36, eNOS, and oxidative damage. Specific inhibition of CD36 prevents glucose-induced oxidative DNA and protein damage in the MVECs. In addition, we have shown for the first time that CD36 may regulate eNOS expression. In summary, upregulation of CD36 and eNOS may lead to increased oxidative stress and reduced NO in diabetes.
Recommended Citation
Farhang Khoee, Hana, "CD36 AND ENDOTHELIAL NITRIC OXIDE SYNTHASE IN ENDOTHELIAL CELL DYSFUNCTION AND DIABETIC CARDIOMYOPATHY" (2006). Digitized Theses. 4879.
https://ir.lib.uwo.ca/digitizedtheses/4879