Document Detail


Angiotensin II modulates interleukin-1β-induced inflammatory gene expression in vascular smooth muscle cells via interfering with ERK-NF-κB crosstalk.
MedLine Citation:
PMID:  21683058     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Angiotensin II is implicated in cardiovascular diseases, which is associated with a role in increasing vascular inflammation. The present study investigated how angiotensin II modulates vascular inflammatory signaling and expression of inducible nitric oxide synthase (iNOS) and vascular cell adhesion molecule (VCAM)-1. In cultured rat aortic vascular smooth muscle cells (VSMCs), angiotensin II suppressed interleukin-1β-induced prolonged phosphorylation of extracellular signal-regulated kinase (ERK) and ribosomal S6 kinase (RSK)-1, and nuclear translocation of nuclear factor (NF)-κB, leading to decreased iNOS but enhanced VCAM-1 expression, associated with an up-regulation of mitogen-activated protein kinase phosphatase-1 expression. Knock-down of RSK1 selectively down regulated interleukin-1β-induced iNOS expression without influencing VCAM-1 expression. In vivo experiments showed that interleukin-1β, iNOS, and VCAM-1 expression were detectable in the aortic arches of both wild-type and apolipoprotein E-deficient (ApoE(-/-)) mice. VCAM-1 and iNOS expression were higher in ApoE(-/-) than in wild type mouse aortic arches. Angiotensin II infusion (3.2 mg/kg/day, for 6 days, via subcutaneous osmotic pump) in ApoE(-/-) mice enhanced endothelial and adventitial VCAM-1 and iNOS expression, but reduced medial smooth muscle iNOS expression associated with reduced phosphorylation of ERK and RSK-1. These results indicate that angiotensin II can differentially modulate inflammatory gene expression in aortic smooth muscle cells through influencing ERK-NF-κB crosstalk, which may contribute to angiotensin II-induced inflammatory disorders related to cardiovascular diseases.
Authors:
Shanqin Xu; Hui Zhi; Xiuyun Hou; Bingbing Jiang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-06-12
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  410     ISSN:  1090-2104     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-07-11     Completed Date:  2011-09-16     Revised Date:  2014-09-18    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  543-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology,  physiology*
Animals
Aorta
Apolipoproteins E / genetics
Cardiovascular Diseases / genetics*,  metabolism
Down-Regulation
Dual Specificity Phosphatase 1 / metabolism
Extracellular Signal-Regulated MAP Kinases / metabolism
Gene Expression Regulation*
Gene Knockdown Techniques
Inflammation / genetics*,  metabolism
Interleukin-1beta / pharmacology,  physiology
Mice
Mice, Mutant Strains
Muscle, Smooth, Vascular / drug effects,  metabolism*
NF-kappa B / metabolism
Nitric Oxide Synthase Type II / metabolism
Rats
Ribosomal Protein S6 Kinases, 90-kDa / metabolism
Vascular Cell Adhesion Molecule-1
Grant Support
ID/Acronym/Agency:
HL083358/HL/NHLBI NIH HHS; R01 HL083358/HL/NHLBI NIH HHS; R01 HL083358-01A2/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Apolipoproteins E; 0/Interleukin-1beta; 0/NF-kappa B; 0/Vascular Cell Adhesion Molecule-1; 11128-99-7/Angiotensin II; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 2.7.11.1/Ribosomal Protein S6 Kinases, 90-kDa; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases; EC 3.1.3.48/Dual Specificity Phosphatase 1
Comments/Corrections

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