Effects of endoplasmic reticulum stress-mediated apoptosis on the pathogenesis of endometriosis
OA: closed
CC0
Abstract
Objective To study the expression levels of glucose-regulated protein 78(GRP-78),glucose-regulated protein 94(GRP-94) and Caspase-12,Caspase-3 in the endometrium of patients with endometriosis(EM),and discuss the effects of endoplasmic reticulum stress-mediated apoptosis on the pathogenesis of endometriosis.Methods Ectopic and eutopic endometrium of 32 patients with EM in Shenyang Fifth People Hospital between Jan.2009 and Dec.2010 were obtained,and 28 normal endometrium were also used for determinations.Apoptotic rates in the endometrium were determined by flow cytometry.GRP78,GRP94,Caspase-12 and Caspase-3 mRNA expression levels were detected by RT-PCR,and GRP78,GRP94,Caspase-12 and Caspase-3 protein expression levels were measured by Western blot.Results Apoptotic rates in the ectopic and eutopic endometrium of patients with EM were significantly higher than that of normal endometrium,and the parameter in ectopic endometrium was also significantly higher than that of eutopic endometrium.GRP78,GRP94,caspase-12 and caspase-3 mRNA expression levels in the ectopic and eutopic endometrium of patients with EM were significantly higher than those of normal endometrium,and these parameters in the ectopic endometrium were also significantly higher than those of eutopic endometrium.Conclusion Apoptosis decreased in the endometrium of patients with EM,and down-regulation of endoplasmic reticulum stress-mediated apoptosis might be one of the mechanisms underlying pathogenesis of endometriosis.
My notes (saved in your browser only)
Condition tags
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.
Source provenance
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0
· commercial use OK