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Am J Physiol Heart Circ Physiol (January 3, 2002). doi:10.1152/ajpheart.00783.2001
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Articles in PresS, published online ahead of print January 3, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00783.2001
Submitted on August 31, 2001
Accepted on December 24, 2001

Protein Kinase C{delta} Modulates Apoptosis Induced by Hyperglycemia in Adult Ventricular Myocytes

Yukitaka Shizukuda1*, Mary E Reyland2, and Peter M Buttrick3

1 Cardiology, University of Illinois at Chicago, Chicago, Illinois
2 Basic Science and Oral Research, University of Colorado Health Sciences Center, Denver, Colorado
3 Cardiology, University of Illinois at Chicago, Chicago, Illinois; Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois

* To whom correspondence should be addressed. E-mail: shizukud{at}uic.edu.

We evaluated the direct effect of hyperglycemia on apoptosis of adult ventricular myocytes (ARVM) in vitro. Hyperglycemia (16.5 mM) for 24 h increased apoptosis by > 3-fold (48.2±4.4%, by TUNEL method) as compared to baseline (14.7±2.5%). Hyperosmolarity with mannitol (11.0 mM) in the presence of 5.5 mM glucose also increased apoptosis by ~2-fold of baseline. Both glucose and mannitol treatment resulted in the membrane translocation of 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{epsilon} specific translocation inhibitor peptide ({epsilon}V1-1) affected neither type of apoptosis. Moderate overexpression of PKC{delta} by adenovirus gene transfer prevented the anti-apoptotic 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 differed from that by hyperosmolarity.




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