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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

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Published on: May 31, 2016

Inhibitor of apoptosis protein survivin regulates vascular injury

Olivier P Blanc-Brude1, Jun Yu, Hector Simosa

  • 1Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.

Nature Medicine
|August 13, 2002
PubMed

Insights

Survivin (Birc5) regulates vascular cell death after arterial injury. Inhibiting this apoptosis pathway may offer new therapies for preventing pathological vessel remodeling.

Area of Science:

  • Molecular biology
  • Cardiovascular research
  • Cellular biology

Background:

  • Survivin (Birc5) is an apoptosis inhibitor involved in cell death prevention and mitosis.
  • Its role in vascular injury remains largely unexplored.
  • The survivin pathway is known to be exploited in cancer.

Purpose of the Study:

  • To investigate the role of survivin in vascular injury.
  • To determine if survivin regulates smooth muscle cell (SMC) apoptosis after arterial injury.
  • To explore the therapeutic potential of targeting the survivin pathway in vascular remodeling.

Main Methods:

  • Balloon-mediated arterial injury in rabbits to assess survivin expression.
  • In vitro studies using cultured SMCs stimulated with serum or PDGF-AB.
  • Adenoviral delivery of a survivin mutant in wire-injured mouse femoral arteries.
  • Assessment of apoptosis, caspase activation, and neointimal formation.

Main Results:

  • Arterial injury induced survivin expression in vascular cells.
  • Survivin suppressed SMC apoptosis and caspase activation in response to PDGF-AB.
  • A phosphorylation-defective survivin mutant reversed PDGF's protective effects, suppressed neointimal formation, and induced apoptosis in vivo.
  • Survivin acts as a critical regulator of SMC apoptosis post-injury.

Conclusions:

  • Survivin is a key regulator of smooth muscle cell apoptosis following acute vascular injury.
  • Targeting the survivin pathway presents a potential therapeutic strategy to mitigate pathological vascular remodeling.

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