Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival.

Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Research Abstract Details 

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Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Abstract Text:

Xiao-ming Liu,Kelly J Peyton,Diana Ensenat,Hong Wang,Mark Hannink,Jawed Alam,William Durante,

OBJECTIVE: Previous studies from our laboratory and others found that NO is a potent inducer of heme oxygenase-1 (HO-1) gene transcription in vascular smooth muscle cells (SMC), however, the mechanism responsible for the induction of HO-1 gene expression has not been elucidated. In the present study, we determined the signaling pathway responsible for the induction of HO-1 and its biological significance. METHODS: Cultured rat aortic SMC were exposed to nitrosative stress by treating cells with various NO donors or with inflammatory cytokines. RESULTS: Nitrosative stress stimulated an increase in HO-1 mRNA expression and promoter activity in vascular SMC. However, mutation of the antioxidant response element (ARE) in the HO-1 promoter or overexpression of a dominant-negative mutant of NF-E2-related factor-2 (Nrf2) abrogated the activation by NO. Electromobility shift assays using an ARE probe detected a complex that was significantly increased in intensity by NO. In addition, the migration of this complex was retarded by using an antibody directed against Nrf2. NO also increased Nrf2 mRNA expression, total and nuclear Nrf2 levels, and the binding of Nrf2 to the HO-1 promoter. Finally, treatment of SMC with NO stimulated apoptosis that was increased by HO-1 inhibition. CONCLUSIONS: These results demonstrate that nitrosative stress induces HO-1 gene transcription through the activation of the Nrf2/ARE complex to counteract NO-induced apoptosis of vascular SMC. The capacity of nitrosative stress to activate Nrf2 and stimulate HO-1 gene transcription may represent a critical adaptive response to maintain cell viability at sites of vascular inflammation and atherosclerosis.

Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Publishing Authors By Initials

XM Liu,KJ Peyton,D Ensenat,H Wang,M Hannink,J Alam,W Durante,

For similar genetic processes: gene expression: transcription, genetic research abstracts see: genetic processes: gene expression: transcription, genetic research

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Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Cardiovascular research

VOLUME: 75

Page Numbers: 381-9

Journal Abbreviation: Cardiovasc. Res.

ISSN: 0008-6363

DAY: 12

MONTH: 03

YEAR: 2007

Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 77427

Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Keywords Mesh Terms:

KEYWORDS: Transcription, Genetic

MESH TERMS: analysis

Chemical & Substance for Abstract: Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival. Information

Substance Name: Heme Oxygenase-1

Registry Number: EC 1.14.99.3

Grant and Affiliation Information for Nitric oxide stimulates heme oxygenase-1 gene transcription via the Nrf2/ARE complex to promote vascular smooth muscle cell survival.

AFFILIATION: Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA.

Country: Netherlands

AGENCY: United States NHLBI

GRANT: HL74996

ACRONYM: HL

MEDLINETA: Cardiovasc Res

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