Document Detail


S100A4/Mts1 produces murine pulmonary artery changes resembling plexogenic arteriopathy and is increased in human plexogenic arteriopathy.
MedLine Citation:
PMID:  14695338     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
S100A4/Mts1 confers a metastatic phenotype in tumor cells and may also be related to resistance to apoptosis and angiogenesis. Approximately 5% of transgenic mice overexpressing S100A4/Mts1 develop pulmonary arterial changes resembling human plexogenic arteriopathy with intimal hyperplasia leading to occlusion of the arterial lumen. To assess the pathophysiological significance of this observation, immunohistochemistry was applied to quantitatively analyze S100A4/Mts1 expression in pulmonary arteries in surgical lung biopsies from children with pulmonary hypertension secondary to congenital heart disease. S100A4/Mts1 was not detected in pulmonary arteries with low-grade hypertensive lesions but was expressed in smooth muscle cells of lesions showing neointimal formation and with increased intensity in vessels with an occlusive neointima and plexiform lesions. Putative downstream targets of S100A4/Mts1 include Bax, which is pro-apoptotic, and the pro-angiogenic vascular endothelial growth factor (VEGF). The increase in S100A4/Mts1 expression precedes heightened expression of Bax in progressively severe neointimal lesions but in non-S100A4/Mts1-expressing cells. VEGF immunoreactivity did not correlate with severity of disease. The relationship of increased S100A4/Mts1 to pathologically similar lesions in the transgenic mice and patients occurs despite differences in localization (endothelial versus smooth muscle cells).
Authors:
Steven Greenway; Robert Jan van Suylen; Gideon Du Marchie Sarvaas; Edwin Kwan; Noona Ambartsumian; Eugene Lukanidin; Marlene Rabinovitch
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of pathology     Volume:  164     ISSN:  0002-9440     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2004 Jan 
Date Detail:
Created Date:  2003-12-25     Completed Date:  2004-02-27     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  253-62     Citation Subset:  AIM; IM    
Affiliation:
Division of Cardiovascular Research, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Animals
Child
Child, Preschool
Endothelium, Vascular / metabolism,  pathology
Female
Gene Expression
Heart Defects, Congenital / complications
Humans
Hypertension, Pulmonary / etiology,  pathology
Immunohistochemistry
Infant
Male
Mice
Mice, Transgenic
Muscle, Smooth, Vascular / metabolism
Proto-Oncogene Proteins / metabolism
Proto-Oncogene Proteins c-bcl-2*
Pulmonary Artery / pathology*
S100 Proteins / biosynthesis*,  genetics
Vascular Endothelial Growth Factor A / metabolism
bcl-2-Associated X Protein
Chemical
Reg. No./Substance:
0/BAX protein, human; 0/Bax protein, mouse; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/S100 Proteins; 0/S100a4 protein, mouse; 0/Vascular Endothelial Growth Factor A; 0/bcl-2-Associated X Protein; 142662-27-9/S100A4 protein, human
Comments/Corrections

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