Document Detail


Chronic high pressure potentiates the antiproliferative effect and abolishes contractile phenotypic changes caused by endothelial cells in cocultured smooth muscle cells.
MedLine Citation:
PMID:  12788664     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
High in vitro pressures have been reported to alter smooth muscle cell (SMC) and endothelial cell (EC) phenotype, while endothelial cells (ECs) can influence the proliferation, phenotype, and contractile features of smooth muscle cells (SMC) in coculture systems. However, little is known about the in vitro effects of pressure on EC/SMC cocultures. We therefore sought to compare SMC proliferation in independent and EC coculture under ambient and high pressure, and identify changes in the contractile phenotype of SMCs by measuring levels of the L-type Ca(2+) channel a(1) subunit (dihydropyridine-DHP receptor) which is critical for Ca(2+) transients, differentiation and contractility in SMC. METHODS: Rat aortic SMCs in independent culture (SMC/0) and coculture with ECs (SMC/EC) were maintained in 5% CO(2) under either atmospheric or high pressure (130 mmHg). SMC were counted at 0, 1, 3, and 5 days and compared to initial cell counts of day 0 before the exposure to experimental conditions. DHP receptor levels were quantitated by Western blotting (three similar studies). RESULTS: ECs suppressed SMC proliferation on day 1 of coculture in both atmospheric and high pressure (20% inhibition vs independent culture, P < or = 0.05). By day 3, cocultured SMC under atmospheric pressure displayed no EC-mediated inhibition, and at day 5, atmospheric cocultured SMCs revealed statistically significant enhanced proliferation as compared with SMCs in independent cultures. However, cocultured SMCs exposed to 130 mmHg pressure displayed sustained sensitivity to EC growth inhibition at both days 3 and 5 of the experiment. Coculture decreased SMC DHP-receptor levels under atmospheric pressure. However, this effect was abolished in cocultures exposed to high pressure. CONCLUSIONS: High pressure substantially alters the regulatory influence of EC on SMC proliferation and contractile potential. This pressure/coculture model should increase our understanding of cellular interaction in hypertensive vasculopathy.
Authors:
Angela G Vouyouka; Shady Selim Salib; Steven Cala; James D Marsh; Marc D Basson
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  The Journal of surgical research     Volume:  110     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  2003 Apr 
Date Detail:
Created Date:  2003-06-05     Completed Date:  2003-07-08     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  344-51     Citation Subset:  IM    
Affiliation:
Departments of Surgery and Cardiology, John D. Dingell VA Medical Center, Detroit, MI 48201-1932, USA. Angela.Vouyouka@med.va.gov
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / cytology,  physiopathology
Calcium / metabolism*
Calcium Channels, L-Type / physiology*
Cell Culture Techniques
Cell Division / physiology
Cell Movement / physiology
Chronic Disease
Coculture Techniques
Endothelium, Vascular / cytology,  physiology*
Hypertension / metabolism,  physiopathology*
Models, Biological
Myocytes, Smooth Muscle / cytology,  physiology*
Phenotype
Pressure
Rats
Vasodilation / physiology*
Chemical
Reg. No./Substance:
0/Calcium Channels, L-Type; 7440-70-2/Calcium

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


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