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Reduced connexin 43 in eutopic endometrium and cultured endometrial stromal cells from subjects with endometriosis

Accumulating evidence indicates that reduced fecundity associated with endometriosis reflects a failure of embryonic receptivity. Microdomains composed of endometrial gap junctions, which facilitate cell-cell communication, may be implicated. Pharmacological or genetic inhibition of connexin (Cx) 43...

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Published in:Molecular human reproduction 2014-03, Vol.20 (3), p.260-270
Main Authors: Yu, Jie, Boicea, Anisoara, Barrett, Kara L, James, Christopher O, Bagchi, Indrani C, Bagchi, Milan K, Nezhat, Ceana, Sidell, Neil, Taylor, Robert N
Format: Article
Language:English
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Summary:Accumulating evidence indicates that reduced fecundity associated with endometriosis reflects a failure of embryonic receptivity. Microdomains composed of endometrial gap junctions, which facilitate cell-cell communication, may be implicated. Pharmacological or genetic inhibition of connexin (Cx) 43 block human endometrial cell differentiation in vitro and conditional uterine deletion of Cx43 alleles cause implantation failure in mice. The aim of this study was to determine whether women with endometriosis have reduced eutopic endometrial Cx43. Cx26 acted as a control. Endometrial biopsies were collected from age, race and cycle phase-matched women without (15 controls) or with histologically confirmed endometriosis (15 cases). Immunohistochemistry confirmed a predominant localization of Cx43 in the endometrial stroma, whereas Cx26 was confined to the epithelium. Cx43 immunostaining was reduced in eutopic biopsies of endometriosis subjects and western blotting of tissue lysates confirmed lower Cx43 levels in endometriosis cases, with Cx43/β-actin ratios=.4±1.5 in control and =1.2±0.3 in endometriosis biopsies (P
ISSN:1360-9947
1460-2407
DOI:10.1093/molehr/gat087