English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Expression of the GABA(A) pi receptor has been described previously in the human endometrium in both luminal epithelium and stroma. Its expression is increased during decidualization in rodents and in the implantation window of human endometrium. Here we localized GABA pi subunit receptor protein in human endometrium and identified regulators of gene expression and activation. GABA(A) pi was localized to the cell surface, and expression increased during the window of embryo implantation in human endometrium. The well-differentiated human endometrial adenocarcinoma cell line Ishikawa was treated with progesterone and transfected with pcDNA-HOXA10, HOXA10 siRNA, or respective controls. GABA(A) pi receptor mRNA expression was evaluated by real-time RT-PCR. Protein expression and localization were evaluated using immunofluorescence. GABA(A) pi receptor mRNA expression was increased significantly after either progesterone treatment or HOXA10 transfection. Coadministration of progesterone along with HOXA10 transfection had no additional effect on the expression of GABA(A) pi receptor mRNA over either agent alone. Blocking HOXA10 expression with siRNA prevented progesterone-induced GABA(A) pi receptor mRNA expression. Additionally, either HOXA10 or progesterone independently caused increased translocation of the GABA receptor from the cytoplasm to the cell membrane. Translocation in response to progesterone was blocked with HOXA10 siRNA. Progesterone-induced GABA(A) pi subunit receptor expression is likely mediated indirectly through progesterone's regulation of HOXA10 expression. Modification of subtype composition and translocation of the GABA receptor ion channel likely modulate endometrial receptivity. Whereas HOXA10 typically enhances the expression of progesterone-responsive genes, here HOXA10 expression leads to production of a less progestin-responsive GABA receptor subtype, likely buffering the effects of luteal phase progesterone on GABA receptor activity.

HOXA10 regulates endometrial GABAAπ receptor expression and membrane translocation

HOXA10 regulates endometrial GABA_Aπ receptor expression and membrane translocation