Implantation markers and endometriosis

Carlo Bulletti, Bulletti C, C Flamigni, Carlo Flamigni, Flamigni C, Dominique de Ziegler, de Ziegler D
Reproductive BioMedicine Online · 2005 · vol. 11(4) , pp. 464–468 · doi:10.1016/s1472-6483(10)61142-x · PMID:16274610 · W2019606157
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This review discusses implantation markers like pinopodes, integrins, and LIF, along with their regulation by hormones and immune cells, and their potential link to endometriosis-associated implantation failure.

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Abstract

The receptive phase of the endometrium seems to occur in close association with the appearance of pinopodes and endometrial integrins that may be activated by the interleukin-1 system (IL-1). Embryo attachment is the result of adhesion protein expression, and the invasion of the embryo is governed by proteolytic enzymes. Leukaemia inhibitory factor (LIF) is produced by natural killer lymphocytes that interact with the invading trophoblast. This may activate urokinase plasminogen activator (uPA) and gelatinase enzymes, which play a crucial role in trophoblast invasion. Oestrogen stimulates, while progesterone inhibits, LIF. The role of endometrial contractility in displacing human embryos from the Fallopian tube to the lumen cavity of the uterus or vagina in terms of pregnancy or wastage is still a matter of discussion. Endometriosis and its associated abnormal uterine contractions may be also linked to implantation failure. Unless new evidence emerges to indicate otherwise, it can be assumed that progesterone is, either in a direct (non-genomic: contractility) or indirect (genomic: decidualization) manner, the only determinant of endometrial priming necessary for embryo nidation.

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Condition tags

endometriosis

MeSH descriptors

Embryo Implantation Endometriosis Interleukin-1 Biomarkers Biomarkers Endometriosis Endometriosis Endometriosis Endometrium Endometrium Estrogens Estrogens Female Fertilization Hormones Hormones Humans Infertility, Female Interleukin-1 Interleukin-6

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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. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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