Histomorphometric alteration and cell-type specific modulation of arylhydrocarbon receptor and estrogen receptor expression by 2,3,7,8-tetrachlorodibenzo-p-dioxin and 17β-estradiol in mouse experimental model of endometriosis

Michio Kitajima, Kitajima M, Khaleque Newaz Khan, Khan KN, Akira Fujishita, Fujishita A, Masuzaki H, Hideaki Masuzaki, Ishimaru T, Tadayuki Ishimaru
Reproductive toxicology (Elmsford, N.Y.) · 2004 · vol. 18(6) , pp. 793–801 · doi:10.1016/j.reprotox.2004.04.012 · PMID:15279877 · W1998585142
article OA: closed CC0 ⤵ 6 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated how TCDD and estradiol alter histomorphometry and aryl hydrocarbon receptor/estrogen receptor expression in specific cell types within a mouse endometriosis model.

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

Abstract

Our purpose was to examine the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), either singly (10 microg/kg) or with 17beta-estradiol (E2, 100 microg/kg), on the growth of endometriosis in a mouse endometriosis model by employing histo-morphometrical analysis as well as expression of arylhydrocarbon receptor (AhR) and estrogen receptor (ER). Epithelial height, stromal thickness, and proliferative activity of the endometriotic lesions were significantly increased by E2 in ovariectomized mice, whereas co-administered TCDD significantly reduced these effects. TCDD alone did not affect the proliferative activity but rather reduced the epithelial height and stromal thickness. ER expression in the luminal epithelium was decreased by E2 compared with ovariectomy alone, while TCDD significantly increased it. On the other hand, stromal ER expression was significantly increased by ovariectomy and decreased by E2, though TCDD did not further enhance this expression. These results indicate that a short-term exposure to TCDD failed to increase the growth of endometriotic lesion and the direct effect of TCDD probably depends on a cell-specific interaction with ovarian steroids mediated by their own receptors. These initial findings in intact tissue of mouse endometriosis may suggest critical roles of steroid hormones in the pathogenesis of endometriosis in relation to endocrine disruptors.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Estradiol Polychlorinated Dibenzodioxins Receptors, Aryl Hydrocarbon Receptors, Estrogen Teratogens Animals Cell Proliferation Cell Proliferation Cell Survival Cell Survival Coloring Agents Endometriosis Estradiol Female Immunohistochemistry Ligands Mice Mice, Inbred Strains Ovariectomy

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 (39)

Cited by (6)

Source provenance

europepmc
last seen: 2026-08-03T06:10:56.557307+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:12:32.173627+00:00
License: CC0 · commercial use OK