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Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis.

Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Research Abstract Details 

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  • Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Abstract Text:

    xiao mei wangXiao Mei Wang,yingze zhangYingze Zhang,hong pyo kimHong Pyo Kim,zhihong zhouZhihong Zhou,carol a feghali-bostwickCarol A Feghali-Bostwick,fang liuFang Liu,emeka ifedigboEmeka Ifedigbo,xiaohui xuXiaohui Xu,tim d ouryTim D Oury,naftali kaminskiNaftali Kaminski,augustine m k choiAugustine M K Choi,

    Idiopathic pulmonary fibrosis (IPF) is a progressive chronic disorder characterized by activation of fibroblasts and overproduction of extracellular matrix (ECM). Caveolin-1 (cav-1), a principal component of caveolae, has been implicated in the regulation of numerous signaling pathways and biological processes. We observed marked reduction of cav-1 expression in lung tissues and in primary pulmonary fibroblasts from IPF patients compared with controls. We also demonstrated that cav-1 markedly ameliorated bleomycin (BLM)-induced pulmonary fibrosis, as indicated by histological analysis, hydroxyproline content, and immunoblot analysis. Additionally, transforming growth factor beta1 (TGF-beta1), the well-known profibrotic cytokine, decreased cav-1 expression in human pulmonary fibroblasts. cav-1 was able to suppress TGF-beta1-induced ECM production in cultured fibroblasts through the regulation of the c-Jun N-terminal kinase (JNK) pathway. Interestingly, highly activated JNK was detected in IPF- and BLM-instilled lung tissue samples, which was dramatically suppressed by ad-cav-1 infection. Moreover, JNK1-null fibroblasts showed reduced smad signaling cascades, mimicking the effects of cav-1. This study indicates a pivotal role for cav-1 in ECM regulation and suggests a novel therapeutic target for patients with pulmonary fibrosis.

    Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Publishing Authors By Initials

    xm wangXM Wang,y zhangY Zhang,hp kimHP Kim,z zhouZ Zhou,ca feghali-bostwickCA Feghali-Bostwick,f liuF Liu,e ifedigboE Ifedigbo,x xuX Xu,td ouryTD Oury,n kaminskiN Kaminski,am choiAM Choi,

    For similar peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta: transforming growth factor beta1 research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: transforming growth factor beta: transforming growth factor beta1 research

    PUBMED ID PMID:

    MEDLINE DATE:

    Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Journal Published:

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

    Journal: The Journal of experimental medicine

    VOLUME: 203

    Page Numbers: 2895-906

    Journal Abbreviation: J. Exp. Med.

    ISSN: 0022-1007

    DAY: 18

    MONTH: 12

    YEAR: 2006

    Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985109

    Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Keywords Mesh Terms:

    KEYWORDS: Transforming Growth Factor beta1

    MESH TERMS: pharmacology

    Chemical & Substance for Abstract: Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis. Information

    Substance Name: Mitogen-Activated Protein Kinase 8

    Registry Number: EC 2.7.1.37

    Grant and Affiliation Information for Caveolin-1: a critical regulator of lung fibrosis in idiopathic pulmonary fibrosis.

    AFFILIATION: Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: R01-HL55330

    ACRONYM: HL

    MEDLINETA: J Exp Med

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

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