Document Detail


Transgenic model of smooth muscle cell cycle reentry: expression pattern of the collageneous matrix.
MedLine Citation:
PMID:  18329551     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: We have previously shown that genetically induced smooth muscle cell (SMC) cycle reentry in transgenic mouse models expressing the SV40 T antigen (TAg) resulted in adaptive arterial remodeling. The present investigation targeted the in vitro expression pattern of the collageneous matrix associated with TAg-induced SMC cycle modulation. METHODS: SMC cultures were established from the transgenic model expressing temperature-sensitive TAg. This allowed inducible transgene expression at the permissive temperature of 33 degrees C compared with the restrictive temperature of 39.5 degrees C. To distinguish a transgene effect from a temperature effect, SMCs with constitutively expressed TAg were used as controls. Data were obtained using array technology, Northern blotting, reverse transcription polymerase chain reaction, and zymography. RESULTS: TAg-induced SMC cycle reentry resulted in significant down-regulation of matrix metalloproteinase (MMP)-3, whereas MMP-2, -9, and -11 were not influenced. In addition, SMC cycle reentry resulted in significantly increased RNA levels of procollagen alpha2(IV), procollagen alpha2(V), and procollagen alpha1(XI), whereas procollagen alpha1(III) and procollagen alpha1(VIII) were down-regulated. Studies of the RNA expression levels of granulocyte-macrophage colony-stimulating factor revealed an up-regulation of this proinflammatory and matrix-modulating cytokine. CONCLUSIONS: This transgenic model provides evidence that TAg-induced cell cycle reentry is associated with a complex modulation of the collageneous matrix. Factors identified in this in vitro study reveal a comprehensive expression pattern of candidates, which might allow the vessel to undergo adaptive arterial remodeling under in vivo conditions. Our results will give rise to further investigations to elaborate on this hypothesis and to improve understanding of the role of such factors in vascular diseases.
Authors:
Jürgen R Sindermann; Christiane Köbbert; Reinhard Voss; Jan Ebbing; Keith L March; Günter Breithardt; Gabriele Weissen-Plenz
Publication Detail:
Type:  Journal Article     Date:  2007-09-12
Journal Detail:
Title:  Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology     Volume:  17     ISSN:  1054-8807     ISO Abbreviation:  Cardiovasc. Pathol.     Publication Date:    2008 Mar-Apr
Date Detail:
Created Date:  2008-03-10     Completed Date:  2008-04-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9212060     Medline TA:  Cardiovasc Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  72-80     Citation Subset:  IM    
Affiliation:
Department of Cardiology and Angiology, University of Münster, 48149 Münster, Germany. sinderm@uni-muenster.de
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Polyomavirus Transforming / genetics,  metabolism
Aorta, Thoracic / cytology
Cell Cycle / physiology*
Cells, Cultured
Collagen / genetics,  metabolism*
Down-Regulation
Gene Expression / physiology*
Gene Expression Profiling
Matrix Metalloproteinase 3 / genetics,  metabolism*
Mice
Mice, Inbred C3H
Mice, Transgenic
Models, Animal
Myocytes, Smooth Muscle / cytology*,  metabolism
Oligonucleotide Array Sequence Analysis
RNA, Messenger / metabolism
Tissue Inhibitor of Metalloproteinase-2 / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Antigens, Polyomavirus Transforming; 0/RNA, Messenger; 127497-59-0/Tissue Inhibitor of Metalloproteinase-2; 9007-34-5/Collagen; EC 3.4.24.17/Matrix Metalloproteinase 3

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


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