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Mol Med Rep. 2011 Sep-Oct;4(5):865-72. doi: 10.3892/mmr.2011.531. Epub 2011 Jul 4.

Proteomic analysis identifies nuclear protein effectors in PKC-delta signaling under high glucose-induced apoptosis in human umbilical vein endothelial cells.

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  • 1Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.

Abstract

Although experimental animal and clinical trials have suggested that additional mechanisms other than protein kinase C (PKC)-β activation are involved in the vascular pathology of diabetic complications, current knowledge on the role of PKC-delta is incomplete and inconclusive. Human umbilical vein endothelial cells (HUVECs) were cultured in both high and normal glucose conditions and infected with recombinant adenovirus to overexpress PKC-delta. PKC-delta expression was also down-regulated using the PKC-delta inhibitor, rottlerin. Using flow cytometric analysis, we showed that PKC-delta is activated and translocates to the nucleus under high glucose conditions. Augmented cell apoptosis and cell cycle arrest were observed in a PKC-delta-dependent manner in the HUVECs. Furthermore, proteomic analyses identified 51 high glucose-induced and PKC-delta-associated proteins, and subsequent matrix-assisted laser desorption/ionization time of flight mass spectrometry analysis uncovered a total of 37 unique proteins. The majority of identified proteins were previously unknown targets of PKC-delta signaling and were involved in the regulation of the cell cycle and apoptosis, tumor suppression, transcription, stress and signal transduction within the nucleus. Our data show that PKC-delta is an important mediator of cell apoptosis and cell cycle arrest in HUVECs under high glucose stress.

[PubMed - indexed for MEDLINE]
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