Redox factor-1 contributes to the regulation of progression from G0/G1 to S by PDGF in vascular smooth muscle cells

Tongrong He; Neal L Weintraub; Prabhat C Goswami; Papri Chatterjee; Dawn M Flaherty; Frederick E Domann; Larry W Oberley

doi:10.1152/ajpheart.01080.2002

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Redox factor-1 contributes to the regulation of progression from G0/G1 to S by PDGF in vascular smooth muscle cells

Journal article

Peer reviewed

Redox factor-1 contributes to the regulation of progression from G0/G1 to S by PDGF in vascular smooth muscle cells

Tongrong He, Neal L Weintraub, Prabhat C Goswami, Papri Chatterjee, Dawn M Flaherty, Frederick E Domann and Larry W Oberley

American journal of physiology. Heart and circulatory physiology, Vol.285(2), pp.H804-812

08/2003

DOI: 10.1152/ajpheart.01080.2002

PMID: 12730053

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Abstract

Redox factor-1 (Ref-1/APE), a multifunctional DNA base excision repair and redox regulation enzyme, plays an important role in oxidative signaling, transcription factor regulation, and cell cycle control. We hypothesized that Ref-1 plays a regulatory role in smooth muscle cell (SMC) proliferation induced by PDGF. Ref-1 antisense oligodeoxynucleotides (AODN), which diminished the level of Ref-1 protein in SMCs by approximately 50%, inhibited PDGF-BB (composed of the homodimer of B-polypeptide chain)-induced [3H]thymidine incorporation compared with control oligodeoxynucleotides. Ref-1 AODN inhibited PDGF-BB-induced S phase entry by approximately 63%, which was overcome by overexpression of Ref-1 by adenoviral-mediated gene transfer. Overexpression of Ref-1 alone without PDGF enhanced SMC entry into the S phase. Furthermore, decreasing Ref-1 protein by treatment of SMCs with Ref-1 AODN, or by immunodepletion of Ref-1 from nuclear extracts, inhibited PDGF-BB-induced activator protein-1 (AP-1) DNA binding activity. Chemical reduction restored the AP-1 DNA binding in Ref-1-depleted nuclear extracts. These results suggest that Ref-1 contributes to the regulation of PDGF-BB-stimulated cell cycle progression from G0/G1 to S in SMCs, with one of the possible steps being redox-regulation of AP-1 by Ref-1 protein.

Muscle, Smooth, Vascular - metabolism

Transcription Factor AP-1 - genetics

Male

G1 Phase - drug effects

Oligoribonucleotides, Antisense - pharmacology

Transcription Factor AP-1 - metabolism

DNA-(Apurinic or Apyrimidinic Site) Lyase

Angiogenesis Inducing Agents - pharmacology

Muscle, Smooth, Vascular - drug effects

Gene Expression

Proto-Oncogene Proteins c-sis

Cells, Cultured

Rats

Platelet-Derived Growth Factor - pharmacology

G1 Phase - physiology

Muscle, Smooth, Vascular - cytology

Rats, Sprague-Dawley

Aorta, Thoracic - cytology

Animals

Resting Phase, Cell Cycle - physiology

Carbon-Oxygen Lyases - genetics

Carbon-Oxygen Lyases - metabolism

S Phase - physiology

Resting Phase, Cell Cycle - drug effects

S Phase - drug effects

Details

Title: Subtitle: Redox factor-1 contributes to the regulation of progression from G0/G1 to S by PDGF in vascular smooth muscle cells
Creators: Tongrong He - Free Radical and Radiation Biology Program, Dept. of Radiation Oncology, The University of Iowa, Iowa City, IA 52242-1181, USA
Neal L Weintraub
Prabhat C Goswami
Papri Chatterjee
Dawn M Flaherty
Frederick E Domann
Larry W Oberley
Resource Type: Journal article
Publication Details: American journal of physiology. Heart and circulatory physiology, Vol.285(2), pp.H804-812
Publisher: United States
DOI: 10.1152/ajpheart.01080.2002
PMID: 12730053
ISSN: 0363-6135
eISSN: 1522-1539
Grant note: CA 66081 / NCI NIH HHS HL 62984 / NHLBI NIH HHS CA 69593 / NCI NIH HHS HL 49264 / NHLBI NIH HHS
Language: English
Date published: 08/2003
Academic Unit: Pulmonary, Critical Care, and Occupational Medicine; Pathology; Surgery; Radiation Oncology; Internal Medicine
Record Identifier: 9984047641202771

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