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Am J Physiol Heart Circ Physiol 282: H1625-H1634, 2002. First published January 3, 2002; doi:10.1152/ajpheart.00783.2001
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Vol. 282, Issue 5, H1625-H1634, May 2002

Protein kinase C-delta modulates apoptosis induced by hyperglycemia in adult ventricular myocytes

Yukitaka Shizukuda1, Mary E. Reyland3, and Peter M. Buttrick1,2

1 Section of Cardiology, Department of Medicine, and 2 Department of Physiology and Biophysics, University of Illinois, Chicago, Illinois 60612; and 3 Department of Basic Science and Oral Research, University of Colorado Health Sciences Center, Denver, Colorado 80282

We evaluated the direct effect of hyperglycemia on apoptosis of adult rat ventricular myocytes (ARVM) in vitro. Hyperglycemia (16.5 mM) for 24 h increased apoptosis by greater than threefold (48.2 ± 4.4%, by the TdT-mediated dUTP nick-end labeling method) compared with baseline (14.7 ± 2.5%). Hyperosmolarity with mannitol (11.0 mM) in the presence of 5.5 mM glucose also increased apoptosis by approximately twofold of baseline. Both glucose and mannitol treatment resulted in the membrane translocation of protein kinase C (PKC)-delta , and the activation of PKC-delta was confirmed by immune complex kinase assay. PKC-delta -specific translocation inhibitor peptide (delta V1-1) attenuated only apoptosis induced by hyperglycemia but not by mannitol. A PKC-varepsilon -specific translocation inhibitor peptide (varepsilon V1-1) affected neither type of apoptosis. Moderate overexpression of PKC-delta by adenovirus gene transfer prevented the antiapoptotic effect of delta V1-1. Furthermore, delta V1-1 attenuated the production of reactive oxygen species (ROS) by glucose. Taken together, our results indicate that increased ROS production regulated by PKC-delta is in part responsible for the induction of apoptosis by hyperglycemia and that apoptosis by hyperglycemia is mechanistically different from that by hyperosmolarity.

reactive oxygen species; glucose; mannitol; antioxidant; adenovirus


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