Augmented Angiogenic Factors Expression via FP Signaling Pathways in Peritoneal Endometriosis

Rakhila H, Halima Rakhila, Al-Akoum M, Mahera Al-Akoum, Mahéra Al-Akoum, Doillon C, Charles Doillon, Charles J. Doillon, Nicolas Lacroix‐Pepin, Lacroix-Pépin N, Nicolas Lacroix-Pépin, Mathieu Lebœuf, Mathieu Leboeuf, Madeleine Lemyre, Lemyre M, Akoum A, Ali Akoum, Marc Pouliot
The Journal of clinical endocrinology and metabolism · 2016 · vol. 101(12) , pp. 4752–4763 · doi:10.1210/jc.2016-1569 · PMID:27726474 · W2530909928
Lab / animal OA: bronze CC0 ⤵ 8 in-corpus citations
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This study investigated how the F-prostanoid receptor pathway influences angiogenesis in peritoneal endometriosis by examining the expression of FP, VEGF, and CXCL8.

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Abstract

CONTEXT: Angiogenesis is required for ectopic endometrial tissue growth. Our previous studies showed that prostaglandin F2α (PGF2α) biosynthetic enzymes and receptor were markedly elevated in endometriotic lesions and that PGF2α is a potent angiogenic factor in endothelial cells. OBJECTIVE: We sought to determine whether or not the F-prostanoid receptor modulates angiogenesis in ectopic stromal cells. DESIGN: Release of angiogenic factors by ectopic endometrial stromal cell primary cultures stimulated with PGF2αand exposed to agents that target PGF2α signaling was assessed. SETTING: The study was conducted in an immunology laboratory at the Centre Hospitalier Universitaire (Québec City) medical research center. PATIENTS: Women found to have peritoneal endometriosis during laparoscopy were included in this study. MAIN OUTCOME MEASURE(S): Prostaglandin E2, PGF2α, vascular endothelial cell growth factor, and CXC chemokine ligand 8 mRNA and protein; FP prostanoid receptor expression. RESULTS: PGF2α markedly up-regulated prostaglandin E2, CXC chemokine ligand 8 and vascular endothelial cell growth factor secretion in endometriotic cells. This effect was suppressed in the presence of a specific F-prostanoid antagonist (AL8810) and its signaling pathway was dependent on F-prostanoid receptor variant. PGF2α can exert its proliferative and angiogenic activities either directly by stimulating endothelial cell proliferation, migration and angiogenesis through F-prostanoid receptor, or indirectly, by stimulating endometriotic stromal cells to produce potent angiogenic factors through either receptor variant. CONCLUSION: These results show for the first time that PGF2α exerts an angiogenic effect on ectopic stromal cells, inducing the secretion of major angiogenic factors via different F-prostanoid signaling pathways. This study suggests a new interpretation of the mechanism underlying endometriosis development involving PGF2α in endometriosis-associated angio-inflammatory changes.

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Condition tags

endometriosis

MeSH descriptors

Angiogenesis Inducing Agents Dinoprost Endometriosis Peritoneal Diseases Receptors, Prostaglandin Signal Transduction Signal Transduction Adult Adult Angiogenesis Inducing Agents Angiogenesis Inducing Agents Angiogenesis Inducing Agents Cells, Cultured Cells, Cultured Dinoprost Dinoprost Dinoprost Endometriosis Endometriosis Female

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 ]

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Cited by (8)

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