Abstract
Objective: In the model of hypoxia/reoxygenation (H/R) injury of cultured rat aortic vascular smooth muscle cells (VSMC), the present study investigated the effects of hypoxic preconditioning (PC) on VSMC and the role of protein kinase C (PKC)-mediated protein phosphorylation in cytoprotective mechanism of hypoxic PC. Results: It was found that hypoxic PC attenuated the sequential H/R injury, including increase of cell viability (86.0±2.6% vs. H/R group: 58.0±5.0%, P <0.01) decrease of intracellular LDH and protein leakage. PKC activator—phorbol-12-myristate-13-acetate (PMA) mimicked, but inhibitor-H 7 or polymyxin B abolished the protective effect of hypoxic PC on H/R injury. Further experiments showed that PC activated PKC (132.0±15.5 vs. control group: 66.0±10.8 pmol Pi/10 6 , P <0.01), increased 32 P incorporation into VSMC and the two strong phosphorylated protein bands appeared in 71 and 31 kDa on PAGE gel. The increase of protein phosphorylation was abolished by incubation with H 7 . Results also showed that BDM (a protein phosphatase activator), abolished, but okadaic acid (protein phosphatase inhibitor) mimicked the protective effect of PC with concomitant attenuation or potentiation of protein phosphorylation respectively. Conclusion: PKC-mediated protein phosphorylation might be an important event of cytoprotective effect of hypoxic PC.
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