| First Author | Fukumoto Y | Year | 2004 |
| Journal | Circulation | Volume | 110 |
| Issue | 14 | Pages | 1953-9 |
| PubMed ID | 15451791 | Mgi Jnum | J:146712 |
| Mgi Id | MGI:3838278 | Doi | 10.1161/01.CIR.0000143174.41810.10 |
| Citation | Fukumoto Y, et al. (2004) Genetically determined resistance to collagenase action augments interstitial collagen accumulation in atherosclerotic plaques. Circulation 110(14):1953-9 |
| abstractText | 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. |
