ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation.

ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Research Abstract Details 

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ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Abstract Text:

Chang-Hoon Woo,Michael P Massett,Tetsuro Shishido,Seigo Itoh,Bo Ding,Carolyn McClain,Wenyi Che,Sreesatya Raju Vulapalli,Chen Yan,Jun-ichi Abe,

Peroxisome proliferator-activated receptors (PPAR) decrease the production of cytokine and inducible nitric-oxide synthase (iNOS) expression, which are associated with aging-related inflammation and insulin resistance. Recently, the involvement of the induction of heme oxygenase-1 (HO-1) in regulating inflammation has been suggested, but the exact mechanisms for reducing inflammation by HO-1 remains unclear. We found that overexpression of HO-1 and [Ru(CO)(3)Cl(2)](2), a carbon monoxide (CO)-releasing compound, increased not only ERK5 kinase activity, but also its transcriptional activity measured by luciferase assay with the transfection of the Gal4-ERK5 reporter gene. This transcriptional activity is required for coactivation of PPARdelta by ERK5 in C2C12 cells. [Ru(CO)(3)Cl(2)](2) activated PPARdelta transcriptional activity via the MEK5/ERK5 signaling pathway. The inhibition of NF-kappaB activity by ERK5 activation was reversed by a dominant negative form of PPARdelta suggesting that ERK5/PPARdelta activation is required for the anti-inflammatory effects of CO and HO-1. Based on these data, we propose a new mechanism by which CO and HO-1 mediate anti-inflammatory effects via activating ERK5/PPARdelta, and ERK5 mediates CO and HO-1-induced PPARdelta activation via its interaction with PPARdelta.

ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Publishing Authors By Initials

CH Woo,MP Massett,T Shishido,S Itoh,B Ding,C McClain,W Che,SR Vulapalli,C Yan,J Abe,

For similar investigative techniques: genetic techniques: gene transfer techniques: transfection research abstracts see: investigative techniques: genetic techniques: gene transfer techniques: transfection research

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ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of biological chemistry

VOLUME: 281

Page Numbers: 32164-74

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 30

MONTH: 08

YEAR: 2006

ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985121

ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Keywords Mesh Terms:

KEYWORDS: Transfection

MESH TERMS: drug effects

Chemical & Substance for Abstract: ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation. Information

Substance Name: Mitogen-Activated Protein Kinase 7

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for ERK5 activation inhibits inflammatory responses via peroxisome proliferator-activated receptor delta (PPARdelta) stimulation.

AFFILIATION: Cardiovascular Research Institute, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL 077789-01A1

ACRONYM: HL

MEDLINETA: J Biol Chem

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