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Bioluminescence Imaging of Heme Oxygenase-1 Upregulation in the Gua Sha Procedure
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Hepatocyte growth factor modulates H2O2-induced mesangial cell apoptosis through induction of heme oxygenase-1

Neetu Radhakrishnan1, Madhu Bhaskaran, Pravin C Singhal

  • 1Department of Medicine, Long Island Jewish Medical Center, New Hyde Park, NY 11042, USA.

Nephron. Physiology
|September 1, 2005
PubMed

Insights

Hydrogen peroxide induces mesangial cell apoptosis via the mitochondrial pathway. Hepatocyte growth factor protects against this injury by upregulating heme oxygenase-1.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oxidative Stress Research

Background:

  • Oxidative stress is a key factor in mesangial cell (MC) injury.
  • Hydrogen peroxide (H2O2) is a significant inducer of MC apoptosis.

Purpose of the Study:

  • To elucidate the molecular mechanisms of H2O2-induced MC apoptosis.
  • To investigate the role of heme oxygenase-1 (HO-1) in hepatocyte growth factor (HGF)-mediated protection against H2O2-induced MC injury.

Main Methods:

  • Assessing mouse MC (MMC) apoptosis induced by H2O2.
  • Analyzing cytochrome c translocation and caspase-9 activity.
  • Evaluating the effects of HGF, hemin, and zinc protoporphyrin on MMC apoptosis and HO-1 expression.

Main Results:

  • H2O2 significantly promoted MMC apoptosis, associated with mitochondrial cytochrome c release and caspase-9 activation, indicating involvement of the mitochondrial pathway.
  • HGF effectively prevented H2O2-induced MMC apoptosis and cytochrome c translocation.
  • HGF upregulated HO-1 expression in MMCs, and hemin demonstrated protective effects, while zinc protoporphyrin blocked HGF's protective influence.

Conclusions:

  • H2O2-induced MC apoptosis is mediated via the mitochondrial pathway.
  • HGF confers protection against H2O2-induced MC injury by inducing HO-1 expression.

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