Document Detail


Time course of right ventricular pressure-overload induced myocardial fibrosis: relationship to changes in fibroblast postsynthetic procollagen processing.
MedLine Citation:
PMID:  22942178     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myocardial fibrillar collagen is considered an important determinant of increased ventricular stiffness in pressure-overload (PO)-induced cardiac hypertrophy. Chronic PO was created in feline right ventricles (RV) by pulmonary artery banding (PAB) to define the time course of changes in fibrillar collagen content after PO using a nonrodent model and to determine whether this time course was dependent on changes in fibroblast function. Total, soluble, and insoluble collagen (hydroxyproline), collagen volume fraction (CVF), and RV end-diastolic pressure were assessed 2 days and 1, 2, 4, and 10 wk following PAB. Fibroblast function was assessed by quantitating the product of postsynthetic processing, insoluble collagen, and levels of SPARC (secreted protein acidic and rich in cysteine), a protein that affects procollagen processing. RV hypertrophic growth was complete 2 wk after PAB. Changes in RV collagen content did not follow the same time course. Two weeks after PAB, there were elevations in total collagen (control RV: 8.84 ± 1.03 mg/g vs. 2-wk PAB: 11.50 ± 0.78 mg/g); however, increased insoluble fibrillar collagen, as measured by CVF, was not detected until 4 wk after PAB (control RV CVF: 1.39 ± 0.25% vs. 4-wk PAB: 4.18 ± 0.87%). RV end-diastolic pressure was unchanged at 2 wk, but increased until 4 wk after PAB. RV fibroblasts isolated after 2-wk PAB had no changes in either insoluble collagen or SPARC expression; however, increases in insoluble collagen and in levels of SPARC were detected in RV fibroblasts from 4-wk PAB. Therefore, the time course of PO-induced RV hypertrophy differs significantly from myocardial fibrosis and diastolic dysfunction. These temporal differences appear dependent on changes in fibroblast function.
Authors:
Catalin F Baicu; Jiayu Li; Yuhua Zhang; Harinath Kasiganesan; George Cooper; Michael R Zile; Amy D Bradshaw
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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:  2012-08-31
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  303     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-05     Completed Date:  2013-01-14     Revised Date:  2013-11-05    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1128-34     Citation Subset:  IM    
Affiliation:
Gazes Cardiac Research Institute, Division of Cardiology, Department of Medicine, Medical University of South Carolina, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / physiology
Cats
Cells, Cultured
Collagen / metabolism
Disease Models, Animal
Fibroblasts / metabolism*,  pathology*
Fibrosis
Hypertrophy, Right Ventricular / complications*,  pathology,  physiopathology
Male
Myocardium / pathology*
Osteonectin / metabolism
Procollagen / metabolism*
Time Factors
Ventricular Dysfunction, Right / complications*,  pathology,  physiopathology
Grant Support
ID/Acronym/Agency:
P01-HL-48788/HL/NHLBI NIH HHS; R01-HL-094517/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Osteonectin; 0/Procollagen; 9007-34-5/Collagen
Comments/Corrections

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