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雌激素受体、血管内皮生长因子和基质金属蛋白酶-2 在血管瘤和血管畸形中的表达
引用本文:刘昱,张端莲,王瑞绵,陈锡昌. 雌激素受体、血管内皮生长因子和基质金属蛋白酶-2 在血管瘤和血管畸形中的表达[J]. 解剖学杂志, 2002, 25(4): 354-359
作者姓名:刘昱  张端莲  王瑞绵  陈锡昌
作者单位:1. 武汉大学医学院组织学与胚胎学教研室,武汉,430071
2. 武汉大学医学院解剖学教研室
摘    要:目的 :探讨雌激素受体 (estrogenreceptor,ER)、血管内皮生长因子 (vascularendothelialgrowthfactor,VEGF)和基质金属蛋白酶 2 (matrixmetalproteinase 2 ,MMP 2 )在血管瘤和血管畸形病理发生中的作用。方法 :对手术切除的血管瘤及血管畸形标本及正常皮肤标本 ,采用免疫组织化学方法检测ER、VEGF、MMP 2的表达 ,做图像分析测定 ,并对 3项指标作相关性分析。结果 :在血管瘤增生期 ,ER、VEGF及MMP 2均有较高表达 ;在血管瘤退化期 ,仅ER有较高表达 ;在血管畸形和正常皮肤对照中 ,ER、VEGF和MMP 2表达极弱。各项指标表达的相关性分析表明血管瘤增生期ER的表达与VEGF的表达呈正相关。结论 :雌激素、VEGF和MMP 2可对血管瘤的病理发生过程发挥作用 ,对血管畸形则无作用。

关 键 词:血管瘤  血管畸形  雌激素受体  血管形成因子

Expression of estrogen receptor and several angiogenesis factors in hemangioma and vascular malformation
LIU Yu,ZHANG Duan-Lian,WANG Rui-Mian,CHEN Xi-Chang. Expression of estrogen receptor and several angiogenesis factors in hemangioma and vascular malformation[J]. Chinese Journal of Anatomy, 2002, 25(4): 354-359
Authors:LIU Yu  ZHANG Duan-Lian  WANG Rui-Mian  CHEN Xi-Chang
Abstract:Objective:To find out the effect of estrogen receptor (ER),vascular endothelial growth factor (VEGF),and matrix metal proteinase-2(MMP-2) on the pathogenesis of hemangioma and vascular malformation.Methods:Fresh operative specimens were collected and were divided into 2 groups:hemangioma and vascular malformation.The specimens of normal skin were also collected.ER,VEGF,MMP-2 were detected by immunohistochemical method.The correlations between the 3 markers were also analyzed.Results:High expressions of ER,VEGF,and MMP-2 were present in proliferating hemangioma.But in the involuting hemangioma,only ER had high expressions.ER,VEGF,and MMP-2 had very weak expressions in vascular malformation and the control.In the proliferating hemangioma,the expression of ER and VEGF had linear positive correlation.Conclusion:Estrogen,VEGF and MMP-2 have effects on the pathogenesis of hemangioma.They may have no effect on vascular malformation.
Keywords:hemangioma  vascular malformation  estrogen receptor  angiogenesis factor  
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