| Role of ageing and coronary atherosclerosis in the development of cardiac fibrosis in the rabbit. | |
| | |
MedLine Citation:
|
PMID: 15537508 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
OBJECTIVE: Myocardial fibrosis contributes to the impairing of cardiac function and characterizes ageing, but is also a consequence of atherosclerotic ischemic disease. Since atherosclerosis is a slow progressive disease, which prevails in elderly populations, the aim of this study was to distinguish the contribution of ageing and atherosclerosis to cardiac fibrosis. METHODS: Coronary atherosclerosis was induced in 5-6-year-old rabbits by a hyperlipemic diet for 9 months. Left ventricular (LV) collagen was quantified by densitometric analysis after Sirius-Red staining; an immunohistochemical investigation of the interstitium was also performed. RESULTS: Atherosclerosis was associated to a marked increase of left ventricular interstitial collagen with the appearance of fibrotic foci and a decrease of coronary vessel endothelial nitric oxide synthase (eNOS) expression. In fibrotic foci, abundant macrophages co-localized with transforming growth factor beta-1 (TGFbeta-1)-positive myofibroblasts and vascular cell adhesion molecule-1 (VCAM-1) positive microvessels (52.3+/-3.9%). In normocholesterolemic rabbits, ageing resulted in a fourfold increase of myocardial interstitial collagen, with alpha-smooth muscle actin and TGFbeta-1 negative fibroblasts and VCAM-1 positive microvessels (19.4+/-1.2%) without macrophages, suggesting a role of endothelial dysfunction in age-related fibrosis. CONCLUSIONS: There is a distinct difference between ageing and coronary atherosclerosis-induced cardiac fibrosis, although the effects may be cumulative. In the cascade of events leading to myocardial remodeling, reparative fibrosis with TGFbeta-1-positive myofibroblasts and interstitial inflammation were the major findings in atherosclerotic old rabbits, whereas with ageing alone, interstitial fibrosis with TGFbeta-1 negative fibroblasts and VCAM-1 positive microvessels prevailed. |
| | |
Authors:
|
Augusto Orlandi; Arianna Francesconi; Marcella Marcellini; Amedeo Ferlosio; Luigi Giusto Spagnoli |
Related Documents
:
|
10381898 - Cosegregation analysis in genetic crosses suggests a protective role for atrial natriur... 22408428 - The -308g/a of tumor necrosis factor (tnf)-α and 825c/t of guanidine nucleotide bindin... 10773228 - Infarct scar: a dynamic tissue. 2091228 - Myocardial connective tissue alterations. 17622948 - Pathophysiology, management, and outcomes of fetal hemodynamic instability during prena... 8450518 - Left ventricular cardiac structure and diastolic function in isolated systolic hyperten... |
Publication Detail:
|
Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Cardiovascular research Volume: 64 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2004 Dec |
Date Detail:
|
Created Date: 2004-11-11 Completed Date: 2005-02-17 Revised Date: 2007-11-15 |
Medline Journal Info:
|
Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
|
Languages: eng Pagination: 544-52 Citation Subset: IM |
Affiliation:
|
Department of Biopathology and Image Diagnostics, Anatomic Pathology Institute, Tor Vergata University of Rome, Via della Ricerca Scientifica, 00133 Rome, Italy. orlandi@uniroma2.it |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Actins
/
analysis,
metabolism Aging / physiology* Animals Cell Count Coronary Artery Disease / metabolism, pathology* Coronary Vessels / pathology Endothelium, Vascular / chemistry, metabolism, pathology* Extracellular Matrix / metabolism, pathology Fibrosis Immunohistochemistry / methods In Situ Nick-End Labeling Male Myocytes, Cardiac / metabolism, pathology* Nitric Oxide Synthase / analysis, metabolism Nitric Oxide Synthase Type III Rabbits Transforming Growth Factor beta / analysis, metabolism Vascular Cell Adhesion Molecule-1 / analysis, metabolism |
| Chemical | |
Reg. No./Substance:
|
0/Actins; 0/Transforming Growth Factor beta; 0/Vascular Cell Adhesion Molecule-1; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Amyloid beta peptides mediate physiological remodelling of the acute O2 sensitivity of adrenomedulla...
Next Document: The neuropsychology of vascular cognitive impairment: is there a specific cognitive deficit?