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Effect of c-myc antisense oligodeoxynucleotides on hypoxia-induced proliferation of pulmonary vascular pericytes

L Wang1, M Xiong, D Che

  • 1Department of Pathology, School of Basic Medical Sciences, Tongji Medical University, Wuhan 430030.

Journal of Tongji Medical University = Tong Ji Yi Ke Da Xue Xue Bao
|February 24, 2001
PubMed

Insights

Hypoxia promotes pulmonary vascular pericyte (PC) proliferation by increasing c-myc gene expression. C-myc antisense oligodeoxynucleotides (ODNs) inhibit this proliferation by downregulating c-myc, offering a potential therapeutic target.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pulmonary Vascular Research

Background:

  • Hypoxia is known to induce cellular changes in the pulmonary vasculature.
  • Pulmonary vascular pericytes (PC) play a crucial role in vascular maintenance and remodeling.
  • The c-myc proto-oncogene is implicated in cell proliferation and differentiation.

Purpose of the Study:

  • To investigate the effect of c-myc antisense oligodeoxynucleotides (ODNs) on hypoxia-induced proliferation of pulmonary vascular pericytes (PC).
  • To determine the role of c-myc gene expression in PC proliferation under hypoxic conditions.

Main Methods:

  • Cell culture of pulmonary vascular pericytes.
  • Dot hybridization for gene expression analysis.
  • 3H-thymidine incorporation assays to measure proliferation.
  • Immunocytochemical techniques to detect PCNA expression.

Main Results:

  • Hypoxia significantly increased c-myc gene expression and PCNA levels in PCs (P < 0.01).
  • Hypoxia also significantly elevated 3H-thymidine incorporation in PCs (P < 0.01).
  • C-myc antisense ODNs significantly inhibited c-myc and PCNA expression (P < 0.05) and 3H-thymidine incorporation (P < 0.01).

Conclusions:

  • Hypoxia promotes pulmonary vascular pericyte proliferation through the upregulation of c-myc gene expression.
  • C-myc antisense ODNs effectively inhibit hypoxia-induced PC proliferation by downregulating c-myc expression.
  • Targeting the c-myc pathway may represent a therapeutic strategy for conditions involving pulmonary vascular remodeling.

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