The poster is one of 89 presentations Joslin scientists will deliver at the ADA Scientific Sessions, to be held Friday, June 10, through Tuesday, June 14 at the San Diego Convention Center. Some 13,000 scientists, physicians and health professionals from around the world will attend the conference, to be held at the San Diego Convention Center. (Abstract Number: 849-P)
"The significance of this study is that we found strong evidence linking chronic activation of a specific form of the PKC enzyme - beta 2 - to the abnormal kidney changes and oxidative stress seen in diabetes," said George L. King, M.D., the study's lead author, Joslin's Director of Research, Head of the Section on Vascular Cell Biology, and a Professor of Medicine at Harvard Medical School. Other investigators in the study included previous Joslin fellows Yutaka Yasuda, M.D., Ph.D., and Noriko Takahara, M.D., as well as Timothy S. Kern, Ph.D., of Case Western Reserve Medical School, Cleveland, Ohio.
Protein kinase C (PKC) is an enzyme essential to the normal functions of the cell and the body. The PKC family of enzymes, which helps regulate many blood vessel functions, comprises about a dozen different molecular forms, or isoforms, including PKC-alpha, PKC-beta 1, PKC-beta 2 and PKC-delta.
In this study, Dr. King and his colleagues proposed that chronic activation or overexpression of the PKC-beta 2 isoform plays an important role in the progression of diabetic kidney disease. To test this hypothesis, researchers used genetic enginee