Extracellularly Signal-Regulated Kinase Activity in the Human Endometrium: Possible Roles in the Pathogenesis of Endometriosis

William Murk, Cem S Atabekoglu, Cem Somer Atabekoğlu, Hakan Cakmak, Hakan Çakmak, Aylin Heper, Aylın Okçu Heper, Arzu Ensari, Arzu Ensarı, Umit A Kayisli, Aydin Arici, Aydın Arıcı
The Journal of clinical endocrinology and metabolism · 2008 · vol. 93(9) , pp. 3532–3540 · doi:10.1210/jc.2007-2051 · PMID:18559923 · W2037059948
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study found that extracellular signal-regulated kinase (ERK) activity is abnormally high in endometriotic endometrial cells, potentially contributing to their survival and pathogenesis.

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Abstract

CONTEXT: Endometriosis is an estrogen-dependent disease characterized by the presence of endometrial tissue outside of the uterine cavity, causing pelvic pain and infertility in 10% of reproductive-aged women. It is unclear why ectopic endometrium remains viable in only a subset of women. ERK1/2 plays key intracellular roles in activating cellular survival and differentiation processes. OBJECTIVE: We sought to determine ERK1/2 activity in patients with endometriosis and its possible roles in regulating endometrial cell survival. DESIGN: ERK1/2 phosphorylation and expression throughout the menstrual cycle were evaluated in vivo in normal and endometriotic human endometrium, and in vitro techniques assessed the steroidal regulation of ERK1/2 and its effect on endometrial cell survival. RESULTS: Total ERK1/2 remained constant in normal and endometriotic endometrium throughout the menstrual cycle. Phospho-ERK1/2 was high in the late proliferative and secretory phases in normal endometrium (P < 0.05). In endometriotic glandular cells, there was no cyclical variation in phospho-ERK1/2. In endometriotic stromal cells, there was also a reduction in phospho-ERK1/2 variation, with higher levels in the early-mid secretory phase (P < 0.05). In cultured endometrial stromal cells (ESCs), estrogen plus progesterone increased ERK1/2 phosphorylation within 15 min (P < 0.05). Although estrogen alone did not induce ERK1/2 phosphorylation in normal ESCs, there was a significant response to estrogen in ESCs isolated from eutopic endometriotic endometrium (P < 0.05). ERK1/2 inhibition in ESCs reduced proliferation and increased apoptosis (P < 0.05). CONCLUSION: Abnormally high levels of ERK1/2 activity may be involved in endometriosis, possibly by stimulating endometrial cell survival.

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Endometrium Extracellular Signal-Regulated MAP Kinases Extracellular Signal-Regulated MAP Kinases Uterine Diseases Cells, Cultured Cell Survival Cell Survival Endometriosis Endometriosis Endometriosis Endometrium Endometrium Enzyme Inhibitors Enzyme Inhibitors Estradiol Estradiol Extracellular Signal-Regulated MAP Kinases Extracellular Signal-Regulated MAP Kinases Female

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