References
Query Results -- Details
MGI Accession ID: MGI:3838278
J Number: J:146712
Other Accession IDs:
Title: Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques.
Authors: Fukumoto Y; Deguchi JO; Libby P; Rabkin-Aikawa E; Sakata Y; Chin MT; Hill CC; Lawler PR; Varo N; Schoen FJ; Krane SM; Aikawa M
Journal: Circulation
Volume: 110
Issue: 14
Date: 2004 Oct 5
Year: 2004
Pages: 1953-9
Review Status: Peer Reviewed
Abstract:
BACKGROUND: We hypothesized that collagenolytic activity produced by activated macrophages contributes to collagen loss and the subsequent instability of atheromatous lesions, a common trigger of acute coronary syndromes. However, no direct in vivo evidence links collagenases with the regulation of collagen content in atherosclerotic plaques. METHODS AND RESULTS: To test the hypothesis that collagenases influence the structure of atheromata, we examined collagen accumulation in atherosclerotic lesions of apolipoprotein E-deficient mice (apoE-/-) that express collagenase-resistant collagen-I (ColR/R/apoE-/-, n=12) or wild-type collagen-expressing mice (Col+/+/apoE-/-, n=12). Aortic atheromata of both groups had similar sizes and numbers of macrophages, a major source of collagenases. However, aortic intimas from ColR/R/apoE-/- mice contained fewer smooth muscle cells, a source of collagen, probably because of decreased migration or proliferation or increased cell death. Despite reduced numbers of smooth muscle cells, atheromata of ColR/R/apoE-/- mice contained significantly more intimal collagen than did those of Col+/+/apoE-/- mice. CONCLUSIONS: These results establish that collagenase action regulates plaque collagen turnover and smooth muscle cell accumulation.
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