The role of prostaglandin E2 in endometriosis

Keith Sacco, Mark Portelli, Joël Pollacco, Pierre Schembri-Wismayer, Jean Calleja-Agius, Jean Calleja‐Agius
Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology · 2011 · vol. 28(2) , pp. 134–138 · doi:10.3109/09513590.2011.588753 · PMID:22003899 · W2109310617
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Prostaglandin E2, upregulated in endometriosis, promotes disease pathophysiology by increasing estrogen synthesis, inhibiting apoptosis, promoting proliferation, and affecting leukocytes and angiogenesis.

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Abstract

Endometriosis is a leading cause of infertility in women of reproductive age. It involves the occurrence of endometrial tissue outside the uterine endometrium, mainly in the peritoneal cavity. Prostaglandin E(2) is up regulated in the peritoneal cavity in endometriosis and is produced by macrophages and ectopic endometrial cells. This prostaglandin is involved in the pathophysiology of the disease and elicits cell signals via four receptor types. Prostaglandin E(2) increases estrogen synthesis by up regulating steroidogenic acute regulatory protein (StAR) and aromatase. It inhibits apoptosis and up regulates fibroblast growth factor-9 (FGF-9) promoting cell proliferation. Prostaglandin E(2) affects leukocyte populations and promotes angiogenesis through its effect on estrogen and up regulation of vascular endothelial growth factor (VEGF). Dienogest is a synthetic progestin targeting expression of genes involved in prostaglandin synthesis.

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Condition tags

endometriosisinfertility

MeSH descriptors

Dinoprostone Endometriosis Apoptosis Apoptosis Cell Proliferation Cell Proliferation Dinoprostone Dinoprostone Endometriosis Endometriosis Endometriosis Estrogens Estrogens Estrogens Female Female Humans Humans Immunosuppression Therapy Immunosuppression Therapy

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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