Document Detail


Activated CD47 promotes pulmonary arterial hypertension through targeting caveolin-1.
MedLine Citation:
PMID:  22215724     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: Pulmonary arterial hypertension (PAH) is a progressive lung disease characterized by pulmonary vasoconstriction and vascular remodelling, leading to increased pulmonary vascular resistance and right heart failure. Loss of nitric oxide (NO) signalling and increased endothelial nitric oxide synthase (eNOS)-derived oxidative stress are central to the pathogenesis of PAH, yet the mechanisms involved remain incompletely determined. In this study, we investigated the role activated CD47 plays in promoting PAH.
METHODS AND RESULTS: We report high-level expression of thrombospondin-1 (TSP1) and CD47 in the lungs of human subjects with PAH and increased expression of TSP1 and activated CD47 in experimental models of PAH, a finding matched in hypoxic human and murine pulmonary endothelial cells. In pulmonary endothelial cells CD47 constitutively associates with caveolin-1 (Cav-1). Conversely, in hypoxic animals and cell cultures activation of CD47 by TSP1 disrupts this constitutive interaction, promoting eNOS-dependent superoxide production, oxidative stress, and PAH. Hypoxic TSP1 null mice developed less right ventricular pressure and hypertrophy and markedly less arteriole muscularization compared with wild-type animals. Further, therapeutic blockade of CD47 activation in hypoxic pulmonary artery endothelial cells upregulated Cav-1, increased Cav-1CD47 co-association, decreased eNOS-derived superoxide, and protected animals from developing PAH.
CONCLUSION: Activated CD47 is upregulated in experimental and human PAH and promotes disease by limiting Cav-1 inhibition of dysregulated eNOS.
Authors:
Philip M Bauer; Eileen M Bauer; Natasha M Rogers; Mingyi Yao; Monica Feijoo-Cuaresma; Joseph M Pilewski; Hunter C Champion; Brian S Zuckerbraun; Maria J Calzada; Jeffrey S Isenberg
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-01-02
Journal Detail:
Title:  Cardiovascular research     Volume:  93     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-02     Completed Date:  2012-09-17     Revised Date:  2013-04-16    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  682-93     Citation Subset:  IM    
Affiliation:
Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anoxia / metabolism,  pathology
Antigens, CD47 / metabolism*
Case-Control Studies
Caveolin 1 / metabolism*
Cells, Cultured
Disease Models, Animal
Endothelium, Vascular / metabolism,  pathology
Humans
Hypertension, Pulmonary / chemically induced,  metabolism*,  pathology
Lung / metabolism*,  pathology
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Monocrotaline / adverse effects
Nitric Oxide Synthase Type III / metabolism
Oxidative Stress / physiology
Rats
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism
Signal Transduction / physiology*
Thrombospondin 1 / deficiency,  genetics,  metabolism
Up-Regulation / physiology*
Grant Support
ID/Acronym/Agency:
K22 CA128616/CA/NCI NIH HHS; P01HL103455/HL/NHLBI NIH HHS; R01 HL-085134/HL/NHLBI NIH HHS; R01 HL-108954/HL/NHLBI NIH HHS; UL1 RR024153/RR/NCRR NIH HHS; UL1 TR000005/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD47; 0/Caveolin 1; 0/Reactive Oxygen Species; 0/Thrombospondin 1; 315-22-0/Monocrotaline; EC 1.14.13.39/Nitric Oxide Synthase Type III
Comments/Corrections
Comment In:
Cardiovasc Res. 2012 Mar 15;93(4):540-2   [PMID:  22311719 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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