The Development of a Mouse Model of Ovarian Endosalpingiosis

Sarah K Bristol-Gould, Christina G Hutten, Christina G. Selkirk, Charles Sturgis, Charles D. Sturgis, Signe M Kilen, Kelly E Mayo, Teresa K Woodruff
Endocrinology · 2005 · vol. 146(12) , pp. 5228–5236 · doi:10.1210/en.2005-0697 · PMID:16141389 · W2159118954
article OA: bronze CC0 ⤵ 5 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

A transgenic mouse model using MIS-Smad2-dn or inhibin alpha-subunit overexpression was developed to study ovarian endosalpingiosis and found that ovarian surface epithelial cells may give rise to the observed cystic structures, suggesting TGF-beta/activin/Smad2 dependence.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

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 Müllerian-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.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Choristoma Cysts Disease Models, Animal Fallopian Tubes Ovarian Diseases Activins Activins Animals Anti-Mullerian Hormone Choristoma Cysts Female Fertility Follicle Stimulating Hormone Follicle Stimulating Hormone Gene Expression Genes, Dominant Gene Targeting Gene Targeting Glycoproteins

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (50)

Cited by (5)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:15:35.797702+00:00
License: CC0 · commercial use OK