MMP1、MMP2、TIMP2在子宫腺肌症异位内膜和在位内膜中的表达

目的 :探讨 MMP1、MMP2、TIMP2在子宫腺肌症异位内膜和在位内膜中的表达情况 ,研究子宫腺肌症的发病机制。方法 :采有免疫组织化学方法检测 MMP1、MMP2、TIMP2在子宫腺肌症异位内膜 40例和在位内膜 40例中的表达。结果 :MMP1在子宫异位内膜腺体中阳性表达率较高 ( 85 % ) ,异位和在位内膜之间有显著性差异 ;MMP2在子宫腺肌症异位和在位内膜间质细胞、腺体中表达一致 ;TIMP2在子宫异位内膜间质中阳性表达率 ( 1 5 % )低于在位内膜间质细胞中阳性表达率 ( 4 0 % ) ,二者有显著性差异。结论 :MMP1可能参与子宫腺肌症的发生、发展 ;MMP2在子宫腺肌症异位和在位内膜间质细胞中均有较强的表达 ,说明子宫腺肌症异位和在位内膜间质细胞具有同源性 ;TIMP2不仅对 MMP2有抑制 ,且对 MMP1也有抑制作用 ,MMPs- TIMPs平衡失调可能有利于子宫腺肌症的发生、发展

Expression of Matrix Metalloproteinases and Tissue Inhibitor of Metalloproteinases in Adenomyosis

Objective:To explore the mechanisms of pathogenesis in adenomyosis. Methods:Immunohistochemistry was induced to investigate the expression of MMP1/MMP2/TIMP2 in fourty cases of ectopic and eutopic endometrium in women with adenomyosis. Results:The expression of MMP1 in glandular epithelial cells of ectopic endometrium was higher(85%) than that of eutopic endometrium (P<0.05);The expression of MMP2 of stromal cells increased simultaneously both in ectopic and eutopic endometrium with adenomyosis; Eutopic endometrium expressed higher levels(40%). Conclusions:The high expression of MMP1 in glandular epithelial cells of ectopic endometrium indicates that MMP1 is involved in genesis and progression of adenomyosis; the similar higher expression of MMP2 of stromal cells both in ectopic and eutopic endometrium with adenomyosis indicates that stromal cells from ectopic and eutopic endometrium have same source;TIMP2 is not only to inhibit MMP2 but also inhibit MMP1 ;An imbalance between MMPs and TIMPs may be involved in the formation and development of adenomyosis.