Involvement of NADPH oxidase and NF-κB activation in CXCL1 induction by vascular endothelial growth factor in human endometrial epithelial cells of patients with adenomyosis

Lai TH, Tsung-Hsuan Lai, Tsung‐Hsuan Lai, Wu PH, Pi-Hui Wu, Pi‐Hui Wu, Wu WB, Wen-Bin Wu, Wen‐Bin Wu
Journal of Reproductive Immunology · 2016 · vol. 118 , pp. 61–69 · doi:10.1016/j.jri.2016.08.011 · PMID:27665197 · W2518044753
Lab / animal OA: closed CC0 ⤵ 10 in-corpus citations
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This study investigated the roles of NADPH oxidase and NF-κB activation in vascular endothelial growth factor-induced CXCL1 expression in human endometrial epithelial cells from adenomyosis patients.

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Abstract

Chemokines were known to participate in inflammation and angiogenesis but have been recently recognized to be involved in embryonic implantation and endometrium-related pathologies. Among these chemokines, the CXC chemokines, such as CXCL1, have potential roles to work as biomarkers to identify patients with uterine adenomyosis. In this study, human endometrial epithelial cells (HEECs) were derived from patients' endometrium with adenomyosis. The inductive effects of CXCL1 production by various mediators/growth factors were investigated in the HEECs. Of the tested mediators, VEGF was found to be the most effective. The immunohistochemistry and RT-PCR analysis revealed a positive staining for VEGF and CXCL1 at the epithelium and the presence of CXCL1 in the human endometrium specimens, respectively. The CXCL1 induction by VEGF could be reduced by the antagonist for VEGF receptor (VEGFR), and by the inhibitors for NADPH oxidase and NF-κB signaling pathway. However, it was not affected by sex hormones and the inhibitors for MAPKs, PI-3K, protein kinase A and C. In parallel, VEGF induced p47 phox NADPH oxidase activation, IκBα phosphorylation, NF-κB translocation and NF-κB-DNA complex formation in the HEECs. Moreover, the CXCL1 released by the HEECs with VEGF stimulation attracted vascular endothelial cell migration. Taken together, we show that VEGF and CXCL1 are expressed in epithelium of the endometrium with adenomyosis and demonstrate here for the first time that VEGF is capable of inducing CXCL1 expression in HEECs through VEGFR, p47 phox NADPH oxidase and NF-κB signaling pathway, which is functionally required for attracting vascular endothelial cell migration.

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Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Chemokine CXCL1 Endometrium Epithelial Cells NADPH Oxidases NF-kappa B Vascular Endothelial Growth Factor A Adenomyosis Adenomyosis Cell Movement Cell Movement Chemokine CXCL1 Chemokine CXCL1 Endometrium Endometrium Endothelium, Vascular Endothelium, Vascular Endothelium, Vascular Epithelial Cells Epithelial Cells

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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 ]

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