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Related Experiment Video

Updated: Jun 22, 2026

Induction and Testing of Hypoxia in Cell Culture
07:01

Induction and Testing of Hypoxia in Cell Culture

Published on: August 12, 2011

RGS5, a hypoxia-inducible apoptotic stimulator in endothelial cells.

Yi Jin1, Xiaojin An, Zelian Ye

  • 1Institute of Molecular Medicine, Peking University, Beijing 100871, China.

The Journal of Biological Chemistry
|July 1, 2009
PubMed
Summary
This summary is machine-generated.

Regulator of G protein signaling 5 (RGS5) is induced by hypoxia in endothelial cells and promotes apoptosis. RGS5 antagonizes vascular endothelial growth factor (VEGF)-induced angiogenesis by activating p38 signaling, suggesting RGS5 as a therapeutic target.

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Induction and Testing of Hypoxia in Cell Culture
07:01

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Published on: August 12, 2011

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
09:17

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

Published on: August 2, 2018

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Physiology

Background:

  • Endothelial cells are crucial for vascular homeostasis and respond to oxygen levels.
  • Regulator of G protein signaling 5 (RGS5) is expressed in vessels but its role in hypoxia is unclear.
  • Hypoxia-inducible factor-1alpha (HIF-1alpha) is a key regulator of cellular response to low oxygen.

Purpose of the Study:

  • To investigate the role of RGS5 in endothelial cells under hypoxic conditions.
  • To elucidate the molecular mechanisms by which RGS5 affects endothelial cell function and angiogenesis.
  • To determine if RGS5 is a potential therapeutic target for vascular diseases.

Main Methods:

  • Human umbilical vein endothelial cells (HUVEC) were exposed to hypoxia and treated with chemical inducers of HIF-1alpha.
  • RGS5 expression, promoter activity, and its effects on cell proliferation and apoptosis were analyzed.
  • Western blotting, Annexin V assay, caspase-3 activity assay, and Matrigel assays were performed.
  • Small interfering RNA (siRNA) and specific inhibitors were used to block RGS5, caspase-3, and p38 signaling.

Main Results:

  • Hypoxia induced RGS5 expression in HUVEC in a HIF-1alpha-dependent manner.
  • RGS5 overexpression reduced HUVEC growth rate and induced apoptosis via caspase-3 activation and increased Bax/Bcl-2 ratio.
  • RGS5 enhanced VEGF-mediated p38 activation but not ERK1/2.
  • RGS5 inhibited VEGF-induced angiogenesis in vitro and in vivo, and promoted apoptosis.

Conclusions:

  • RGS5 is a novel hypoxia-induced gene regulated by HIF-1.
  • RGS5 promotes endothelial cell apoptosis and antagonizes VEGF-mediated angiogenesis.
  • RGS5 represents a potential therapeutic target for modulating angiogenesis and treating vascular pathologies.