Document Detail

Substrate-induced phenotypic switches of human smooth muscle cells: an in vitro study of in-stent restenosis activation pathways.
MedLine Citation:
PMID:  21106574     Owner:  NLM     Status:  MEDLINE    
In-stent restenosis is a clinical complication following coronary angioplasty caused by the implantation of the metal device in the atherosclerotic vessel. Histological examination has shown a clear contribution of both inflammatory and smooth muscle cells (SMCs) to the deposition of an excess of neointimal tissue. However, the sequence of events leading to clinically relevant restenosis is unknown. This paper aims to study the phenotype of SMCs when adhering on substrates and exposed to biochemical stimuli typical of the early phases of stent implantation. In particular, human SMC phenotype was studied when adhering on extracellular matrix-like material (collagen-rich gel), thrombus-like material (fibrin gel) and stent material (stainless steel) in the presence or absence of a platelet-derived growth factor (PDGF) stimulus. Cells on the collagen and fibrin-rich substrates maintained their contractile phenotype. By contrast, cells on stainless steel acquired a secretory phenotype with a proliferation rate 50 per cent higher than cells on the natural substrates. Cells on stainless steel also showed an increase in PDGF-BB receptor expression, thus explaining the increase in proliferation observed when cells were subject to PDGF-BB stimuli. The stainless steel substrate also promoted a different pattern of β1-integrin localization and an altered expression of hyaluronan (HA) synthase isoforms where the synthesis of high-molecular-weight HA seemed to be favoured. These findings highlighted the induction of a phenotypic pattern in SMC by the stainless steel substrate whereby the formation of a HA-rich neointimal tissue is enhanced.
Anna L Guildford; Helen J S Stewart; Christopher Morris; Matteo Santin
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Publication Detail:
Type:  In Vitro; Journal Article     Date:  2010-11-24
Journal Detail:
Title:  Journal of the Royal Society, Interface / the Royal Society     Volume:  8     ISSN:  1742-5662     ISO Abbreviation:  J R Soc Interface     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-03-23     Completed Date:  2011-07-15     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  101217269     Medline TA:  J R Soc Interface     Country:  England    
Other Details:
Languages:  eng     Pagination:  641-9     Citation Subset:  IM    
School of Pharmacy and Biomolecular Sciences, University of Brighton, Huxley Building, Lewes Road, Brighton BN2 4GJ, UK.
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MeSH Terms
Antigens, CD29 / metabolism
Cell Adhesion
Cell Proliferation
Cells, Cultured
Collagen / chemistry
Coronary Restenosis
Extracellular Matrix / metabolism
Gene Expression Regulation
Glucuronosyltransferase / chemistry
Myocytes, Smooth Muscle / cytology*
Platelet-Derived Growth Factor / metabolism
Proto-Oncogene Proteins c-sis
Surface Properties
Time Factors
Reg. No./Substance:
0/Antigens, CD29; 0/Platelet-Derived Growth Factor; 0/Proto-Oncogene Proteins c-sis; 0/platelet-derived growth factor BB; 9007-34-5/Collagen; EC; EC synthase

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