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Sci Rep. 2017 Aug 15;7(1):8289. doi: 10.1038/s41598-017-08840-y.
2
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N Engl J Med. 2017 Jul 6;377(1):28-40. doi: 10.1056/NEJMoa1700089. Epub 2017 May 19.
3
Endometrial Stromal and Epithelial Cells Exhibit Unique Aberrant Molecular Defects in Patients With Endometriosis.子宫内膜间质细胞和上皮细胞在子宫内膜异位症患者中表现出独特的异常分子缺陷。
Reprod Sci. 2018 Jan;25(1):140-159. doi: 10.1177/1933719117704905. Epub 2017 May 11.
4
Progesterone resistance in endometriosis: origins, consequences and interventions.子宫内膜异位症中的孕激素抵抗:起源、后果及干预措施
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G蛋白偶联受体CXCR7在人和小鼠子宫内膜异位症中过表达。

G-Protein-Coupled Receptor CXCR7 Is Overexpressed in Human and Murine Endometriosis.

作者信息

Pluchino Nicola, Mamillapalli Ramanaiah, Moridi Irene, Tal Reshef, Taylor Hugh S

机构信息

1 Department of Obstetrics, Gynecology and Reproductive Sciences, Yale School of Medicine, New Haven, CT, USA.

出版信息

Reprod Sci. 2018 Aug;25(8):1168-1174. doi: 10.1177/1933719118766256. Epub 2018 Mar 27.

DOI:10.1177/1933719118766256
PMID:29587613
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6346303/
Abstract

Endometriosis is a chronic inflammatory disease. Dysfunctional regulation of chemokines and chemokine receptors is a crucial aspect of endometriosis pathogenesis. Chemokine G-protein-coupled receptors (GPCRs) are important drug targets that regulate inflammation and immunity. Recently, CXCR7, a C-X-C motif containing GPCR, has been identified as a receptor for chemokine ligand CXCL12, one of the best characterized chemokines for cell trafficking, angiogenesis, and cell proliferation in cancer and inflammation. Here, we investigated the expression and localization of CXCR7 in human endometriosis and a murine model of the disease. Normal endometrial epithelium and stroma showed undetectable or very low expression of CXCR7, without any significant changes across phases of the menstrual cycle in humans. CXCR7 is significantly upregulated in endometriosis, showing higher staining in glands and in associated vessels. The mouse model recapitulated the human findings. In conclusion, overexpression of CXCR7 in different cellular populations of endometriosis microenvironment may play a role in the pathogenesis and represent a novel target for treatment.

摘要

子宫内膜异位症是一种慢性炎症性疾病。趋化因子和趋化因子受体的功能失调调控是子宫内膜异位症发病机制的一个关键方面。趋化因子G蛋白偶联受体(GPCRs)是调节炎症和免疫的重要药物靶点。最近,CXCR7,一种含有GPCR的C-X-C基序,已被鉴定为趋化因子配体CXCL12的受体,CXCL12是癌症和炎症中细胞迁移、血管生成和细胞增殖方面特征最明显的趋化因子之一。在此,我们研究了CXCR7在人类子宫内膜异位症及该疾病小鼠模型中的表达和定位。正常子宫内膜上皮和基质显示CXCR7表达不可检测或极低,在人类月经周期各阶段无任何显著变化。CXCR7在子宫内膜异位症中显著上调,在腺体和相关血管中染色更强。小鼠模型重现了人类的研究结果。总之,CXCR7在子宫内膜异位症微环境不同细胞群体中的过表达可能在发病机制中起作用,并代表一个新的治疗靶点。