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Related Experiment Videos

Heme oxygenase-1 expression levels are cell cycle dependent.

C Colombrita1, G Lombardo, G Scapagnini

  • 1Department of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.

Biochemical and Biophysical Research Communications
|August 21, 2003
PubMed
Summary

Heme oxygenase-1 (HO-1) protects endothelial cells from angiotensin II (Ang II)-induced DNA damage by upregulating in the G(0)/G(1) phase. This stress response is crucial for controlled cell growth.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Heme oxygenase-1 (HO-1) is a stress-inducible protein implicated in cellular defense against oxidative injury.
  • Angiotensin II (Ang II) is a known inducer of oxidative stress in endothelial cells.

Purpose of the Study:

  • To investigate the role of human HO-1 in cell-cycle progression.
  • To determine the effect of Ang II on HO-1 gene expression in endothelial cells at different cell-cycle phases.

Main Methods:

  • Human endothelial cells were cultured in serum-deprived (G(0)/G(1) phase) or exponentially growing (10% FBS) conditions.
  • Ang II was added to stimulate HO-1 expression, and its levels were measured via protein activity and mRNA using real-time RT-PCR.
  • Oxidative damage was assessed by measuring 8-epi-isoprostane PGF(2 alpha) generation.

Related Experiment Videos

  • HO-1 inhibition was achieved using Stannic mesoporphyrin (SnMP).

    • Main Results:

    • Ang II significantly increased HO-1 protein and activity in a time-dependent manner in G(0)/G(1) phase cells, with peak levels at 16 hours.
    • HO-1 mRNA levels were elevated by Ang II as early as 1 hour in G(0)/G(1) cells, with higher induction rates in serum-starved cells compared to continuously growing cells.
    • Ang II increased 8-epi-isoprostane PGF(2 alpha) generation, and HO-1 inhibition potentiated this effect and Ang II-mediated DNA damage.

    Conclusions:

    • HO-1 expression in the G(0)/G(1) phase plays a critical role in attenuating Ang II-induced DNA damage during cell-cycle progression.
    • Upregulation of HO-1 generates bilirubin and carbon monoxide (CO) to counteract Ang II-mediated oxidative DNA damage.
    • The inducibility of HO-1 in the G(0)/G(1) phase is essential for controlled cell growth and is likely regulated by a complex system involving reactive oxygen species.