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Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
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Nox5 mediates PDGF-induced proliferation in human aortic smooth muscle cells

Desmond B Jay1, Christopher A Papaharalambus, Bonnie Seidel-Rogol

  • 1Department of Medicine, Emory University, Atlanta, GA 30322, USA.

Free Radical Biology & Medicine
|May 10, 2008
PubMed

Insights

Reactive oxygen species (ROS) from NADPH oxidase 5 (Nox5) drive vascular smooth muscle cell proliferation. Inhibiting Nox5 reduces ROS production and cell growth, highlighting Nox5

Area of Science:

  • Vascular biology
  • Cell signaling
  • Molecular medicine

Background:

  • Vascular smooth muscle cell (VSMC) proliferation is a key factor in vascular disease development.
  • Platelet-derived growth factor (PDGF) stimulates VSMC proliferation via signaling pathways involving reactive oxygen species (ROS).
  • NADPH oxidases (NOX) are a source of cellular ROS, with Nox5 being a potential regulator in VSMCs.

Purpose of the Study:

  • To investigate the specific role of Nox5 in PDGF-stimulated human aortic smooth muscle cell (HASMC) proliferation.
  • To elucidate the contribution of Nox5-derived ROS to PDGF-induced signaling and cell growth.

Main Methods:

  • Cultured HASMCs were treated with PDGF and either N-acetyl cysteine (NAC) or a JAK inhibitor (AG490).
  • Specific knockdown of Nox5 was achieved using small interfering RNA (siRNA).
  • ROS production, HASMC proliferation, and JAK/STAT pathway phosphorylation (JAK2, STAT3) were measured.

Main Results:

  • Nox5 isoforms were expressed in HASMCs.
  • NAC pretreatment significantly reduced PDGF-induced HASMC proliferation.
  • PDGF-stimulated proliferation was abolished by the JAK inhibitor AG490.
  • Nox5 knockdown reduced PDGF-induced ROS production and HASMC proliferation.
  • Nox5 siRNA also inhibited PDGF-stimulated JAK2 and STAT3 phosphorylation.

Conclusions:

  • Nox5-derived ROS are critical mediators of PDGF-induced JAK/STAT activation.
  • Nox5 plays a significant role in regulating PDGF-stimulated human aortic smooth muscle cell proliferation.
  • Targeting Nox5 may offer a therapeutic strategy for vascular diseases characterized by VSMC proliferation.

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