title: [A pathomorphological study on atherosclerotic regression with references between apoptosis and atherosclerotic plaque with central depression in rabbit aorta].
abstract: Atherosclerotic plaque with central depression (depressed lesions) have been proposed as one morphological feature of atherosclerotic regression in the elderly. We have also revealed that depressed lesions have been found not only in the aorta of elderly human but also in rabbit aorta. In this study a relationship between apoptosis and atherosclerotic regression was immunohistochemically studied to clarify the possibility of the pathogenesis of depressed lesion in rabbit aorta. Twenty male New Zealand White rabbit (NZW) were fed with a 1.0% cholesterol diet during a 12-week atherogenic induction period. Then they were fed only with a basic diet for 36-week (n = 6) and 48-week (n = 6, experimental group) regression periods. A control group was fed with 1.0% cholesterol diet for 12-week (n = 2) and 60-week (n = 6). They were killed and aortas were fixed with formalin. Sections obtained from aortas were processed for histological and immunohistochemical studies including the TUNEL method, staining with Ki-67 and others. Several depressed lesions were found in the aortas of NZW animal, but none were noted in control aortas. Results of surface involvement in the experimental groups were significantly lower than in the control, and the aortas of the experimental group had atherosclerotic regression. Apoptosis was found in the depressed lesions, which had more apoptotic cells than non-regressed atherosclerotic plaques. Furthermore, the apoptotic cells were significantly greater in the center of depressed lesions than in marginal areas. Ki-67 staining was positive in the atherosclerotic plaque, but negative in the depressed lesions. It appears that the NZW aortic atherosclerotic plaques may transform to depressed lesions with apoptosis. Atherosclerotic regression has been associated with apoptosis.
authors.affiliation: Department of Pathology, Nihon University School of Medicine, Tokyo.
authors.forename: K
authors.initials: K
authors.lastname: Takashi
authors.forename: T
authors.initials: T
authors.lastname: Oinuma
authors.forename: T
authors.initials: T
authors.lastname: Yamada
mesh_terms: D000818:Animals; D001011:Aorta / Q000473:pathology*; D017209:Apoptosis; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology*; D004036:Diet, Atherogenic; D008297:Male; D011817:Rabbits