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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 被引量:11

Expression of estrogen receptor and several angiogenesis factors in hemangioma and vascular malformation
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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。 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.
出处 《解剖学杂志》 CAS CSCD 北大核心 2002年第4期354-359,共6页 Chinese Journal of Anatomy
关键词 血管瘤 血管畸形 雌激素受体 血管形成因子 hemangioma vascular malformation estrogen receptor angiogenesis factor
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  • 1周德凯,中华小儿外科杂志,1991年,12卷,713页
  • 2Zhang M H,Am J Pathol,1995年,149卷,6期,1559页
  • 3刘文英,中华小儿外科杂志,1997年,18卷,71页
  • 4周德凯,中华小儿外科杂志,1991年,12卷,71页
  • 5Sasaki G H,Plast Reconstr Surg,1984年,73卷,359页
  • 6刘文英,张尚福,胡廷泽,韦福康,高艳,成娘.小儿血管瘤性激素受体检测[J].中华小儿外科杂志,1997,18(2):71-73. 被引量:4
  • 7周德凯,王赞尧.婴幼儿血管瘤血清雌二醇水平的研究[J].中华小儿外科杂志,1991,12(2):71-72. 被引量:13

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