| Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. | |
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MedLine Citation:
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PMID: 11463726 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To obtain information on the molecular and cellular mechanisms of flow-induced arterial remodeling, we analyzed the morphology and smooth muscle cell (SMC) characteristics in rat mesenteric resistance arteries after interventions that decreased and increased flow. Juvenile male Wistar Kyoto rats were subjected to surgery that, compared with control arteries, provided arteries with chronic low flow and chronic high flow. Low flow resulted in a decreased passive lumen diameter, hypotrophy of the artery wall, and both loss and decreased size of SMCs. Time course studies, with intervention length ranging from 2 to 32 days of altered blood flow, showed that the narrowing of the lumen diameter in low-flow arteries appeared within 2 days and that an early dedifferentiation of SMC phenotype was indicated by markedly reduced levels of desmin mRNA. High flow resulted in an increased passive lumen diameter and in hypertrophy of the artery wall. The hypertrophy resulted from SMC proliferation because SMC number, measured by the 3D-dissector technique, was increased and immunohistochemical assessment of proliferating cell nuclear antigen also showed an increase. The widening of high-flow arteries required 16 days to become established, at which time desmin mRNA was reduced. This time was also required to establish changed wall mass in both low-flow and high-flow arteries. Apoptotic cells detected by TdT-mediated dUTP-biotin nick end labeling staining were mainly located in the medial layer, and evaluation of DNA fragmentation indicated that increased apoptosis occurred in both low flow and high flow. This study shows for the first time direct evidence that reduced and elevated blood flow in resistance arteries produce, respectively, decrease and increase in SMC number, with dedifferentiation of the SMCs in both cases. |
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Authors:
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C L Buus; F Pourageaud; G E Fazzi; G Janssen; M J Mulvany; J G De Mey |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Circulation research Volume: 89 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2001 Jul |
Date Detail:
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Created Date: 2001-07-20 Completed Date: 2001-08-30 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 180-6 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, The Netherlands. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / genetics Blood Flow Velocity Cell Division Cell Size DNA Fragmentation Desmin / genetics Immunohistochemistry In Situ Nick-End Labeling Male Mesenteric Arteries / metabolism, physiology* Muscle, Smooth, Vascular / chemistry, cytology* Proliferating Cell Nuclear Antigen / analysis RNA, Messenger / genetics, metabolism Rats Rats, Inbred WKY Stress, Mechanical Time Factors Vascular Resistance |
| Chemical | |
Reg. No./Substance:
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0/Desmin; 0/Proliferating Cell Nuclear Antigen; 0/RNA, Messenger |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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