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Selenium suppressed hydrogen peroxide‐induced vascular smooth muscle cells calcification through inhibiting oxidative stress and ERK activation

Atherosclerosis is frequently associated with vascular calcification. Increasing evidences underline that the essential micronutrient selenium may prevent atherosclerosis, but the role of selenium in vascular calcification remains unknown. In this study, we assessed the effect of sodium selenite (Na2SeO3) on H2O2‐enhanced vascular smooth muscle cells (VSMCs) calcification and examined the involvement of extracellular signal‐regulated kinase (ERK) signaling pathway. Hydrogen peroxide enhanced vascular calcification by inducing osteoblastic differentiation of VSMCs, as showed by up‐regulating the mRNA expression of type I collagen, osteocalcin, and Runx2, a key transcription factor for osteoblastic differentiation, increasing alkaline phosphatase activity, and calcium deposition. These effects of H2O2 were suppressed by pretreatment of the cells with selenite (0.1–1 µM) for 24 h. In addition, H2O2 activated the phosphorylation of ERK1/2 and inhibition of H2O2‐activated ERK signaling by MEK inhibitor PD98059 blocked the effect of H2O2 on osteoblastic differentiation of VSMCs. Furthermore, H2O2 induced oxidative stress in calcifying VSMCs, as evidenced by the increase of intracellular reactive oxygen species production and malondialdehyde level, and the decrease of total protein thiols content and the activity of antioxidant selenoenzyme glutathione peroxidases. Selenite pretreatment also attenuated H2O2‐induced oxidative stress and ERK activation. These results suggested that selenite suppressed H2O2‐enhanced osteoblastic differentiation and calcification of VSMCs through inhibiting oxidative stress and ERK activation, indicating a potential preventive role for selenium in vascular calcification. J. Cell. Biochem. 111: 1556–1564, 2010. © 2010 Wiley‐Liss, Inc.