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ARID1A 蛋白和 PGR 蛋白在子宫内膜中相互作用，并在子宫内膜异位症中呈现正相关。

ARID1A and PGR proteins interact in the endometrium and reveal a positive correlation in endometriosis.

机构信息

Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI, 49503, USA.

Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI, 49503, USA; Life Science Institute, Repure Life Science, Seoul, 03722, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2021 Apr 23;550:151-157. doi: 10.1016/j.bbrc.2021.02.144. Epub 2021 Mar 9.

DOI:10.1016/j.bbrc.2021.02.144
PMID:33706098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8005488/
Abstract

Endometriosis is a disorder in which endometrial cells normally limited to the lining of the uterus proliferate outside the uterine cavity and can cause pelvic pain and infertility. ARID1A levels are significantly reduced in the eutopic endometrium from women with endometriosis. Uterine specific Arid1a knock-out mice were infertile due to loss of epithelial progesterone receptor (PGR) signaling. However, the functional association of ARID1A and PGR in endometriosis has not been studied. We examined the expression patterns and co-localization of ARID1A and PGR in eutopic endometrium from women with and without endometriosis using immunostaining and Western blot analysis. ARID1A and PGR proteins co-localized in the epithelium during the proliferative and the early secretory phases. Our immunoprecipitation analysis and proximity ligation assay (PLA) revealed physical interaction between ARID1A and PGR-A but not PGR-B in the mouse and human endometrium. ARID1A levels positively correlated with PGR levels in the eutopic endometrium of women with endometriosis. Our results bring new perspectives on the molecular mechanisms involved in endometrial receptivity and progesterone resistance in endometriosis. The interrelationship between ARID1A and PGR may contribute to explaining the non-receptive endometrium in endometriosis-related infertility.

摘要

子宫内膜异位症是一种病症，其中子宫内膜细胞通常局限于子宫内层，在子宫腔外增殖，并可能导致盆腔疼痛和不孕。患有子宫内膜异位症的女性的在位子宫内膜中 ARID1A 水平显著降低。由于上皮孕激素受体 (PGR) 信号的丧失，子宫特异性 Arid1a 敲除小鼠不育。然而，ARID1A 和 PGR 在子宫内膜异位症中的功能关联尚未研究。我们使用免疫染色和 Western blot 分析检查了来自患有和不患有子宫内膜异位症的女性的在位子宫内膜中 ARID1A 和 PGR 的表达模式和共定位。ARID1A 和 PGR 蛋白在增殖期和早期分泌期在上皮细胞中共定位。我们的免疫沉淀分析和接近连接分析 (PLA) 显示 ARID1A 和 PGR-A 而不是 PGR-B 在小鼠和人子宫内膜中存在物理相互作用。患有子宫内膜异位症的女性在位子宫内膜中 ARID1A 水平与 PGR 水平呈正相关。我们的结果为涉及子宫内膜容受性和孕激素抵抗的分子机制提供了新的视角。ARID1A 和 PGR 之间的相互关系可能有助于解释与子宫内膜异位症相关不孕中的非接受性子宫内膜。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/696926f63eb5/nihms-1681580-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/6613c30e657d/nihms-1681580-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/993ac93bec49/nihms-1681580-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/769912c3bb31/nihms-1681580-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/696926f63eb5/nihms-1681580-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/6613c30e657d/nihms-1681580-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/993ac93bec49/nihms-1681580-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/769912c3bb31/nihms-1681580-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d73e/8005488/696926f63eb5/nihms-1681580-f0004.jpg

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Endometriosis.子宫内膜异位症。
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