Katsuda S, Okada Y, Nakanishi I
Department of Pathology, School of Medicine, Kanazawa University, Ishikawa, Japan.
Exp Mol Pathol. 1990 Feb;52(1):13-24. doi: 10.1016/0014-4800(90)90054-h.
We examined the correlation between elastolysis and abnormal accumulation of microfibrils in the arteries of rabbits using light and electron microscopic and tissue culture techniques. Partial constriction of the common carotid arteries of rabbits gave rise to gradual atrophy of the media with elastolysis and an unusual accumulation of microfibrils. With advancing experimental atherosclerosis in cholesterol-fed rabbits, the elastofibrotic intima generally became thick and hyalinized and was replaced by bundles of microfibrils lacking elastin or associated with only tiny elastin aggregates and disrupted elastic fibers. Organ cultures of aortic explants from rabbits with or without pancreatic elastase supplementation for 5 days disclosed that there was complete loss of medial elastic fibers and increasing deposition of microfibrils, morphologically identical to elastin-associated microfibrils, around viable smooth muscle cells only in the elastase supplemented group. These observations suggest that abnormal accumulation of microfibrils in the elastic tissue is closely associated with excessive elastolysis of preformed or newly formed elastic fibers during elastic tissue remodeling. Enhanced synthesis of microfibrils may occur in response to elastolysis as a reparative phenomenon.
我们运用光学显微镜、电子显微镜及组织培养技术,研究了兔动脉中弹性蛋白溶解与微原纤维异常积聚之间的相关性。兔颈总动脉部分狭窄会导致中膜逐渐萎缩,伴有弹性蛋白溶解和微原纤维异常积聚。在喂食胆固醇的兔中,随着实验性动脉粥样硬化的进展,弹性纤维增生性内膜通常会变厚并玻璃样变,被缺乏弹性蛋白的微原纤维束取代,或仅与微小的弹性蛋白聚集体及断裂的弹性纤维相关。对有或没有补充胰弹性蛋白酶5天的兔主动脉外植体进行器官培养发现,仅在补充弹性蛋白酶的组中,中膜弹性纤维完全丧失,且在存活的平滑肌细胞周围微原纤维沉积增加,其形态与弹性蛋白相关的微原纤维相同。这些观察结果表明,在弹性组织重塑过程中,弹性组织中微原纤维的异常积聚与预先形成或新形成的弹性纤维的过度弹性蛋白溶解密切相关。作为一种修复现象,微原纤维的合成增强可能是对弹性蛋白溶解的反应。