Document Detail


Alterations in cultured myocardial fibroblast function following the development of left ventricular failure.
MedLine Citation:
PMID:  16516916     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A structural event in the progression of left ventricular (LV) failure is myocardial extracellular matrix (ECM) remodeling. The myocardial fibroblast is a major cell type influencing the ECM, but whether and to what degree specific phenotypic differences in myocardial fibroblasts can be demonstrated to occur in culture with the development of LV failure remains unclear. Adult pigs (25 kg) were used for control myocardial fibroblast preparations (N=5) or following pacing-induced LV failure (N=5; 240 bpm, 3 weeks). LV remodeling occurred with pacing as evidenced by increased LV end diastolic volume (132+/-11 vs. 60+/-4 mL for control; P<0.05). Functional parameters including migration, adhesion, collagen and matrix metalloproteinase release were assessed in fibroblast cultures from passages 1-4. The following findings were consistent with each passage and the results were analyzed with control values set to 100%. Migration of LV failure fibroblasts increased by over 170% (P<0.05). Adhesion to collagen I, laminin and fibronectin was increased by over 160% in LV failure fibroblasts (P<0.05). beta(1) integrin density decreased by 50% in LV failure fibroblasts (P<0.05). Fibrillar collagen release increased by over 130% and matrix metalloproteinase-2 increased by 140% in LV failure fibroblasts (P<0.05). The unique findings of this study are two-fold. First, after a pathological stimulus in-vivo, adult myocardial fibroblasts maintain a consistent phenotype through early passages in-vivo. Second, a differential release of, and response to ECM components occurred in LV failure fibroblasts. Thus, a phenotypic transformation of the myocardial fibroblast occurs with the development of LV failure, which in turn may contribute to matrix remodeling and presents as a potential cellular therapeutic target.
Authors:
English C Flack; Merry L Lindsey; Christina E Squires; Brooke S Kaplan; Robert E Stroud; Leslie L Clark; Patricia G Escobar; William M Yarbrough; Francis G Spinale
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2006-03-06
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  40     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-03-27     Completed Date:  2006-06-13     Revised Date:  2014-02-12    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  474-83     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cells, Cultured
Collagen Type I / metabolism
Extracellular Matrix / metabolism*,  pathology
Fibroblasts / metabolism*,  pathology
Fibronectins / metabolism
Laminin / metabolism
Myocardium / metabolism*,  pathology
Swine
Ventricular Dysfunction, Left / metabolism*,  pathology
Ventricular Remodeling*
Grant Support
ID/Acronym/Agency:
HL-59165/HL/NHLBI NIH HHS; HL-75360/HL/NHLBI NIH HHS; HL-97012/HL/NHLBI NIH HHS; P01-HL48788/HL/NHLBI NIH HHS; R01 HL075360/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Collagen Type I; 0/Fibronectins; 0/Laminin

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


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