CIAPIN1 siRNA inhibits proliferation, migration and promotes apoptosis of VSMCs by regulating Bcl-2 and Bax

Curr Neurovasc Res. 2013 Feb;10(1):4-10. doi: 10.2174/156720213804805909.

Abstract

Migration, proliferation and apoptosis of vascular smooth muscle cells (VSMCs) have recently been identified as important processes in a variety of human vascular diseases, including atherosclerosis, arterial injury, and restenosis after angioplasty. These processes are regulated by interactions between the local cell-cell and cytokine environment. Cytokine induced apoptosis inhibitor (CIAPIN1) is a novel antiapoptotic molecule and plays a vitally important role in malignant phenotypes of cancers. However, the effect of CIAPIN1 on VSMCs has not been reported. In the present study, we constructed the adenovirus encoding CIAPIN1 siRNA and transduced it into VSMCs. The results demonstrated that CIAPIN1 siRNA inhibited proliferation, migration and promotes apoptosis of VSMCs by regulating Bcl-2 and Bax. Our results suggest that CIAPIN1 siRNA might play the key role in VSMC biological function and provide the new therapeutic strategy for vascular diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology*
  • Caspase 3 / metabolism
  • Cell Movement / physiology*
  • Cell Proliferation*
  • Cells, Cultured
  • Humans
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / metabolism*
  • Myocytes, Smooth Muscle / cytology
  • Myocytes, Smooth Muscle / metabolism*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • RNA, Small Interfering
  • bcl-2-Associated X Protein / metabolism*

Substances

  • CIAPIN1 protein, human
  • Intracellular Signaling Peptides and Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Small Interfering
  • bcl-2-Associated X Protein
  • Caspase 3