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学科主题: 临床医学
题名:
C-Jun NH2-Terminal Kinase and p38 Inhibition Suppresses Prostaglandin E2-Stimulated Aromatase and Estrogen Receptor Levels in Human Endometriosis
作者: Zeng, Cheng; Xu, Jia-ning; Zhou, Yan; Yang, Hui-xia; Zhou, Ying-fang; Xue, Qing
刊名: JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
发表日期: 2015-11-01
DOI: 10.1210/jc.2015-2031
卷: 100, 期:11, 页:E1404-E1414
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism
研究领域[WOS]: Endocrinology & Metabolism
关键词[WOS]: ROSTRAL VENTROLATERAL MEDULLA ; ACTIVATED PROTEIN-KINASES ; BRAIN-STEM DEATH ; PROGESTERONE-RECEPTOR ; BREAST-CANCER ; PROLIFE ROLE ; CYCLIC-AMP ; CELLS ; EXPRESSION ; DIFFERENTIATION
英文摘要:

Context: Endometriosis isanestrogen-dependent disease. P38 and C-jun NH2-terminal kinase (JNK) inhibitors may have a therapeutic effect on endometriosis through regulation of prostaglandin E2 (PGE2)-induced estrogen metabolism.

Objective: The objective of this study was to determine whether the activated MAPKs signaling pathway observed in human ectopic endometrial stromal cells (ESCs) from ovarian endometriomas influences levels of aromatase and estrogen receptor beta (ER beta) protein regulated by PGE2. In turn, the effects of inhibiting MAPKs in the presence of PGE2 on estrogen production were investigated in vitro and in vivo.

Results: Expression of aromatase and ER beta regulated by PGE2 were much higher in ESCs than eutopic ESCs from the same person. Activation of p38, JNK, ERK 1/2 and ERK 5 MAPKs by PGE2 were observed in ESCs, where PGE2-stimulated aromatase and ER beta expression mainly through p38 and JNK pathway. P38 and JNK inhibition or small interfering RNA knockdown blocked PGE2-induced aromatase and ER beta expression. PGE2 enhanced binding of downstream p38 and JNK transcription factors activating transcription factor-2 and c-Jun to aromatase and ERB promoter regions in ESCs. Moreover, treatment of endometriosis xenografts with inhibitors of p38 and JNK abrogated PGE2-amplified estradiol synthesis and xenograft growth.

Conclusions: PGE2 activates p38 and JNK signaling pathways, further stimulating c-Jun and activating transcription factor-2 binding to aromatase and ERB promoter regions with elevated estradiol production. Inhibition of JNK and P38 may be a potential method of treating human endometriosis.

语种: 英语
所属项目编号: 81270674 ; 7132204
项目资助者: National Natural Science Foundation of China ; Beijing Municipal Natural Science Foundation
WOS记录号: WOS:000364925700014
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/60208
Appears in Collections:北京大学第一临床医学院_期刊论文

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作者单位: Peking Univ, Hosp 1, Dept Obstet & Gynecol, Beijing 100034, Peoples R China

Recommended Citation:
Zeng, Cheng,Xu, Jia-ning,Zhou, Yan,et al. C-Jun NH2-Terminal Kinase and p38 Inhibition Suppresses Prostaglandin E2-Stimulated Aromatase and Estrogen Receptor Levels in Human Endometriosis[J]. JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM,2015,100(11):E1404-E1414.
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