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人子宫内膜间质细胞对细胞外基质的黏附增强:子宫内膜异位症发病机制的一个可能机制。

Attachment to extracellular matrices is enhanced in human endometriotic stromal cells: a possible mechanism underlying the pathogenesis of endometriosis.

机构信息

Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Yufu-shi, Oita, Japan.

出版信息

Eur J Obstet Gynecol Reprod Biol. 2011 Mar;155(1):85-8. doi: 10.1016/j.ejogrb.2010.10.026. Epub 2010 Nov 26.

DOI:10.1016/j.ejogrb.2010.10.026
PMID:21112686
Abstract

OBJECTIVE

Endometriosis is characterized by the ectopic growth of endometrial tissue. One of the first steps to the spread of endometriosis in the peritoneal cavity is the attachment of endometriotic cells to peritoneal surfaces after they have been released into the peritoneal fluid from pre-existing endometriotic lesions. The increased adhesive and proliferative potential of endometriotic cells in response to specific extracellular matrix (ECM) components has been suggested to contribute to the pathogenesis of endometriosis.

STUDY DESIGN

Adhesive properties of endometriotic stromal cells (ECSC) and normal eutopic endometrial cells (NESC) to various extracellular matrix proteins were investigated by in vitro cell adhesion assays. The expression levels of integrins in these cells were also examined by Western blot analysis.

RESULTS

Both ECSC and NESC significantly adhered to collagen type I and collagen type IV. ECSC revealed higher adhesive properties to these ECM proteins than NESC did. ECSC, but not NESC, adhered to fibronectin and laminin. Higher levels integrin of α1, α2, αv, β1, and β3 protein expression were observed in ECSC than in NESC. On the other hand, the levels of integrin α3 and αL proteins were lower in ECSC than in NESC.

CONCLUSIONS

The results suggest that endometriotic cells possess stronger adhesion to ECM proteins, and that increase may be mediated, in part, through integrins. These findings may elucidate one of the mechanisms underlying the formation of peritoneal endometriotic lesions.

摘要

目的

子宫内膜异位症的特征是子宫内膜组织的异位生长。子宫内膜异位症在腹腔内扩散的第一步是,在先前存在的子宫内膜异位病灶中,子宫内膜细胞释放到腹腔液后,附着在腹膜表面。子宫内膜异位症细胞对特定细胞外基质 (ECM) 成分的黏附性和增殖潜能增加,被认为有助于子宫内膜异位症的发病机制。

研究设计

通过体外细胞黏附试验研究了子宫内膜异位症基质细胞 (ECSC) 和正常在位子宫内膜细胞 (NESC) 对各种细胞外基质蛋白的黏附特性。还通过 Western blot 分析检查了这些细胞中整合素的表达水平。

结果

ECSC 和 NESC 均显著黏附于 I 型和 IV 型胶原。ECSC 对这些 ECM 蛋白的黏附特性高于 NESC。ECSC 而非 NESC 黏附于纤连蛋白和层粘连蛋白。在 ECSC 中观察到更高水平的整合素 α1、α2、αv、β1 和 β3 蛋白表达,而在 NESC 中则较低。另一方面,ECSC 中的整合素 α3 和 αL 蛋白水平低于 NESC。

结论

这些结果表明,子宫内膜异位症细胞对 ECM 蛋白具有更强的黏附性,这种增加可能部分通过整合素介导。这些发现可能阐明了形成腹膜子宫内膜异位病灶的机制之一。

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