The development of a mouse model of ovarian endosalpingiosis

被引:48
作者
Bristol-Gould, SK
Hutten, CG
Sturgis, C
Kilen, SM
Mayo, KE
Woodruff, TK
机构
[1] Northwestern Univ, Dept Neurobiol & Physiol, Evanston, IL 60208 USA
[2] Northwestern Univ, Dept Biochem Mol Biol & Cell Biol, Evanston, IL 60208 USA
[3] Northwestern Univ, Ctr Reprod Sci, Evanston, IL 60208 USA
[4] Evanston NW Hosp, Evanston, IL 60208 USA
[5] Northwestern Univ, Dept Med, Feinberg Sch Med, Chicago, IL 60611 USA
[6] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA
关键词
D O I
10.1210/en.2005-0697
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Pelvic pain is a common presenting ailment in women often linked to ovulation, endometriosis, early pregnancy, ovarian cancer, and cysts. Clear differential diagnosis for each condition caused by these varied etiologies is difficult and may slow the delivery of therapy that, in the case of ovarian cancer, could be fatal. Ovarian endosalpingiosis, a pelvic condition typified by the presence of cystic glandular structures lined by benign tubal/salpingeal epithelium, is also associated with pelvic pain in women. The exact cellular antecedents of these epithelial lined cystic structures are not known, nor is there a known link to ovarian cancer. A mouse model of ovarian endosalpingiosis has been developed by directing a dominant-negative version of the TGF-beta transcription factor, Smad2, to the ovary using the Mullerian-inhibiting substance promoter (MIS-Smad2-dn). Female mice develop an ovarian endosalpingeal phenotype as early as 3 months of age. Importantly, cysts continuous with the ovarian surface epithelial have been identified, indicating that these cyst cells may be derived from the highly plastic ovarian surface epithelial cell layer. A second transgenic mouse model that causes loss of activin action (inhibin alpha-subunit transgenic mice) develops similar cystic structures, supporting a TGF-beta/activin/Smad2 dependence in the onset of this disease.
引用
收藏
页码:5228 / 5236
页数:9
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