Regulation of reactive-oxygen-species generation in fibroblasts by Rac1

Maitrayee Sundaresan; Zu-Xi Yu; Victor J Ferrans; David J Sulciner; Silvio Gutkind; Kaikobad J Irani; Pascal J Goldschmidt-Clermont; Toren Finkel

doi:10.1042/bj3180379

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Regulation of reactive-oxygen-species generation in fibroblasts by Rac1

Journal article

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Peer reviewed

Regulation of reactive-oxygen-species generation in fibroblasts by Rac1

Maitrayee Sundaresan, Zu-Xi Yu, Victor J Ferrans, David J Sulciner, Silvio Gutkind, Kaikobad J Irani, Pascal J Goldschmidt-Clermont and Toren Finkel

The Biochemical journal, Vol.318(Pt 2), pp.379-382

09/01/1996

DOI: 10.1042/bj3180379

PMCID: PMC1217632

PMID: 8809022

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Abstract

In a variety of non-phagocytic cell types, there is a marked increase in intracellular levels of reactive oxygen species (ROS), including superoxide and H2O2, after ligand stimulation. We demonstrate that in NIH 3T3 cells transient expression of constitutively activated forms of the small GTP-binding proteins Ras or Rac1 leads to a significant increase in intracellular ROS. An increase in intracellular ROS is also demonstrated after growth factor [platelet-derived growth factor (PDGF) or epidermal growth factor (EGF)] or cytokine [tumour necrosis factor-alpha (TNF-alpha) or interleukin (IL)-1 beta] stimulation of NIH 3T3 cells. Expression of a dominant negative allele of Rac1 inhibits the rise in ROS seen after Ras expression or after stimulation by either growth factors or cytokines. These results provide the first demonstration of the pathway by which ligand stimulation of ROS occurs in non-phagocytic cells and suggest that the family of Ras-related small GTP-binding proteins may function as regulators of the intracellular redox state.

Details

Title: Subtitle: Regulation of reactive-oxygen-species generation in fibroblasts by Rac1
Creators: Maitrayee Sundaresan - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Zu-Xi Yu - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Victor J Ferrans - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
David J Sulciner - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Silvio Gutkind - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Kaikobad J Irani - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Pascal J Goldschmidt-Clermont - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Toren Finkel - Cardiology Branch, NHLBI, NIH, Bethesda, MD 20892-1650, USA
Resource Type: Journal article
Publication Details: The Biochemical journal, Vol.318(Pt 2), pp.379-382
DOI: 10.1042/bj3180379
PMID: 8809022
PMCID: PMC1217632
NLM abbreviation: Biochem J
ISSN: 0264-6021
eISSN: 1470-8728
Language: English
Date published: 09/01/1996
Academic Unit: Cardiovascular Medicine; Radiation Oncology; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
Record Identifier: 9984047869002771

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