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001-es BibID:	BIBFORM023026
Első szerző:	Cheng, Caroline
Cím:	Heme Oxygenase 1 Determines Atherosclerotic Lesion Progression Into a Vulnerable Plaque / Cheng, C., Noordeloos, A. M., Jeney, V., Soares, M. P., Moll, F., Pasterkamp, G., Serruys, P. W., Duckers, H. J.
Dátum:	2009
ISSN:	0009-7322
Megjegyzések:	Background-The molecular regulation for the transition from stable to vulnerable plaque remains to be elucidated. Heme oxygenase 1 (HO-1) and its metabolites have been implicated in the cytoprotective defense against oxidative injury in atherogenesis. In this study, we sought to assess the role of HO-1 in the progression toward plaque instability in carotid artery disease in patients and in a murine model of vulnerable plaque development. Methods and Results-Atherectomy biopsy from 112 patients with clinical carotid artery disease was collected and stratified according to characteristics of plaque vulnerability. HO-1 expression correlated closely with features of vulnerable human atheromatous plaque (P<0.005), including macrophage and lipid accumulation, and was inversely correlated with intraplaque vascular smooth muscle cells and collagen deposition. HO-1 expression levels correlated with the plaque destabilizing factors matrix metalloproteinase-9, interleukin-8, and interleukin-6. Likewise, in a vulnerable plaque model using apolipoprotein E(-/-) mice, HO-1 expression was upregulated in vulnerable versus stable lesions. HO-1 induction by cobalt protoporphyrin impeded lesion progression into vulnerable plaques, indicated by a reduction in necrotic core size and intraplaque lipid accumulation, whereas cap thickness and vascular smooth muscle cells were increased. In contrast, inhibition of HO-1 by zinc protoporphyrin augmented plaque vulnerability. Plaque stabilizing was prominent after adenoviral transduction of HO-1 compared with sham virus-treated animals, providing proof that the observed effects on plaque vulnerability were HO-1 specific. Conclusions-Here we demonstrate in a well-defined patient group and a murine vulnerable plaque model that HO-1 induction reverses plaque progression from a vulnerable plaque to a more stable phenotype as part of a compensatory atheroprotective response.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Circulation. - 119 : 23 (2009), p. 3017-3027. -
További szerzők:	Noordeloos, Annemarie M. Jeney Viktória (1971-) (vegyész, kémia tanár) Soares, Miguel P. Moll, Frans Pasterkamp, Gerard Serruys, Patrick W. Duckers, Henricus J.
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