The extracellular signal‐regulated kinase 1/2 triggers angiogenesis in human ectopic endometrial implants by inducing angioblast differentiation and proliferation

Sefa Arlıer, Sefa Arlier, William Murk, Ozlem Guzeloglu-Kayisli, Ozlem Guzeloglu‐Kayisli, Nihan Semerci, Kellie Larsen, Mehmet S Tabak, Mehmet Selcuk Tabak, Aydın Arıcı, Aydin Arici, Frederick Schatz, Charles J Lockwood, Umit A. Kayisli
American journal of reproductive immunology (New York, N.Y. : 1989) · 2017 · vol. 78(6) · doi:10.1111/aji.12760 · PMID:28921734 · W2755066066
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Abstract

PROBLEM: The role of extracellular signal-regulated kinase (ERK)1/2-mediated angiogenesis during endometriotic nidation is unknown. We posit that ERK1/2-induced angioblast differentiation and proliferation promotes ectopic endometrial angiogenesis. METHODS OF STUDY: ), cytokines, normal peritoneal fluid (NPF) or endometriotic peritoneal fluid (EPF) ±PD98059, an ERK1/2 inhibitor, treaded primary human endometrial endothelial cells (HEECs) were evaluated by T-/P-ERK1/2 immunoblotting, MTT viability and tube formation assays. RESULTS: HEECs exhibited higher endothelial P-ERK1/2 immunoreactivity in ectopic vs eutopic endometria. Double-immunostained ectopic endometria displayed abundant CD34-positive angioblasts exhibiting strong P-ERK1/2 and PCNA immunoreactivity. EPF and vascular growth factor (VEGF)-A significantly increased HEEC proliferation and P-ERK1/2 levels. PD98059 reduced basal, EPF, and VEGF-induced HEEC proliferation and promoted vascular stabilization following tube formation. CONCLUSION: induces proliferation to trigger ectopic endometrial angiogenesis.

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mesh:D004715

MeSH descriptors

Choristoma Endometriosis Endometrium Endothelial Cells Extracellular Signal-Regulated MAP Kinases Neovascularization, Pathologic Cell Differentiation Cell Proliferation Cells, Cultured Choristoma Endometriosis Endometrium Endothelial Cells Extracellular Signal-Regulated MAP Kinases Female Humans Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factor A

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