Extracellularly signal-regulated kinase activity in the human endometrium: possible roles in the pathogenesis of endometriosis

Murk W, William Murk, Cem S Atabekoglu, Atabekoglu CS, Cem Somer Atabekoğlu, Hakan Cakmak, Hakan Çakmak, Cakmak H, Aylın Okçu Heper, Aylin Heper, Heper A, Arzu Ensarı, Arzu Ensari, Ensari A, Umit A. Kayisli, Kayisli UA, Aydin Arici, Arici A, 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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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 Cells, Cultured Cell Survival Cell Survival Cell Survival Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Enzyme Inhibitors Enzyme Inhibitors Enzyme Inhibitors

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (41)

Cited by (37)

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