Chinese Journal of Tissue Engineering Research ›› 2010, Vol. 14 ›› Issue (20): 3646-3649.doi: 10.3969/j.issn.1673-8225.2010.20.009

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Effect of osteopontin antisense nucleotide on proliferation of rat vascular smooth muscle cells

Li Hui, Liu Qi-feng, Liu Gui-nan   

  1. Department of Cardiology, the First Hospital of China Medical University, Shenyang  110001, Liaoning Province, China
  • Online:2010-05-14 Published:2010-05-14
  • Contact: Liu Gui-nan, Master, Professor, Department of Cardiology, the First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China guinanliu@hotmail.com
  • About author:Li Hui, Studying for master’s degree, Department of Cardiology, the First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China lihui242yy@sohu.com
  • Supported by:

    the National Natural Science Foundation of China, No. 30871074*

Abstract:

BACKGROUND: The expression of osteopontin (OPN) is obviously up-regulated in neointimal formation after vessel damage and promotes the proliferation and migration of vascular smooth muscle cells (VSMCs) and adventitial cells.

OBJECTIVE: To explore the effect of OPN antisense nucleotide on proliferation of rat vascular smooth muscle cells.

METHODS: A10 aortic VSMCs of rat were cultured. The effects of OPN antisense nucleotide on proliferation of VSMCs were observed by MTT colorimetric assay. Flow cytometry was performed to track cell cycle progression. RT-PCR was done to detect the effect of VSMCs transfected OPN antisense nucleotide on the antigen expression of proliferated cells.

RESULTS AND CONCLUSION: OPN antisense nucleotide significantly inhibited VSMCs proliferation, but the inhibitory rate was decreased with time prolonged. OPN antisense nucleotide blocked VSMCs cycle in G0/G1 phase, and inhibited the proliferation of VSMCs. Compared with the control group, the antigen expression of proliferated cells were decreased obviously in the OPN antisense nucleotide group (P < 0.05). Accordingly, OPN antisense nucleotide can block VSMCs cycle in G0/G1 phase, thus, inhibits the proliferation of VSMCs and suppresses the vascular intima hyperplasia.

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