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Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function
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RNA interference-mediated survivin gene knockdown induces growth arrest and reduced migration of vascular smooth

Christoph S Nabzdyk1, Hope Lancero, Khanh P Nguyen

  • 1Division of Vascular and Endovascular Surgery, Laboratory for Accelerated Vascular Research, University of California, San Francisco, CA 94143, USA.

American Journal of Physiology. Heart and Circulatory Physiology
|August 23, 2011
PubMed

Insights

RNA interference targeting Survivin (SVV) in vascular smooth muscle cells (VSMCs) halts proliferation and migration without causing cell death. This suggests SVV RNAi may prevent vascular injury responses.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cell Biology
  • Vascular Biology

Background:

  • Survivin (SVV) is a multifunctional protein involved in neointimal hyperplasia.
  • Nuclear SVV is critical for mitosis, while mitochondrial SVV offers cytoprotection.

Purpose of the Study:

  • To investigate the impact of RNA interference (RNAi)-mediated SVV knockdown on vascular smooth muscle cells (VSMCs).
  • To assess effects on cell cycle, apoptosis, migration, and gene expression in human saphenous vein VSMCs.

Main Methods:

  • SVV knockdown achieved using small interfering RNA (siRNA) or short hairpin RNA (shRNA) lentiviral transduction.
  • Quantitative PCR confirmed >75% reduction in SVV gene expression.
  • Cell cycle analysis, transwell migration assays, and apoptosis assays (flow cytometry) were performed.

Main Results:

  • SVV knockdown significantly increased p53 and p27 protein levels.
  • VSMC proliferation and migration were inhibited, with cell cycle arrest at G(2)/M phase.
  • Nuclear SVV was targeted more effectively than mitochondrial SVV; apoptosis was not induced.

Conclusions:

  • RNAi-mediated SVV knockdown causes cell cycle arrest and impairs chemotaxis in VSMCs without cytotoxicity.
  • Differential regulation of nuclear and mitochondrial SVV pools impacts mitosis and apoptosis.
  • Targeting SVV with RNAi may limit vascular injury responses without vessel destabilization.

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