The motile and invasive capacity of human endometrial stromal cells: implications for normal and impaired reproductive function

Charlotte H E Weimar, Nick Macklon, Nick S Macklon, Emiel D Post Uiterweer, Jan J Brosens, Birgit Gellersen
Human reproduction update · 2013 · vol. 19(5) , pp. 542–557 · doi:10.1093/humupd/dmt025 · PMID:23827985 · W2126195456
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Human endometrial stromal cell migration and invasion are controlled by complex signaling pathways and contribute to implantation, tissue remodeling, and reproductive disorders like endometriosis and recurrent pregnancy loss.

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Abstract

BACKGROUND Mechanisms underlying early reproductive loss in the human are beginning to be elucidated. The migratory and invasive capacity of human endometrial stromal cells (ESCs) is increasingly recognized to contribute to the intense tissue remodelling associated with embryo implantation, trophoblast invasion and endometrial regeneration. In this review, we examine the signals and mechanisms that control ESC migration and invasion and assess how deregulation of these cell functions contributes to common reproductive disorders. METHODS The PubMed database was searched for publications on motility and invasiveness of human ESCs in normal endometrial function and in reproductive disorders including implantation failure, recurrent pregnancy loss (RPL), endometriosis and adenomyosis, covering the period 2000-2012. RESULTS Increasing evidence suggests that implantation failure and RPL involve abnormal migratory responses of decidualizing ESCs to embryo and trophoblast signals. Numerous reports indicate that endometriosis, as well as adenomyosis, is associated with increased basal and stimulated invasiveness of ESCs and their progenitor cells, suggesting a link between a heightened menstrual repair response and the formation of ectopic implants. Migration and invasiveness of ESCs are controlled by a complex array of hormones, growth factors, chemokines and inflammatory mediators, and involve signalling through Rho GTPases, phosphatidylinositol-3-kinase and mitogen-activated protein kinase pathways. CONCLUSIONS Novel concepts are extending our understanding of the key functions of ESCs in effecting tissue repair imposed by cyclic menstruation and parturition. Migration of decidualizing ESCs also serves to support blastocyst implantation and embryo selection through discriminate motile responses directed by embryo quality. Targeting regulatory molecules holds promise for developing new strategies for the treatment of reproductive disorders such as endometriosis and recurrent miscarriage; and harnessing the migratory capacity of progenitor mesenchymal stem cells in the endometrium may offer new opportunities in regenerative medicine.

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Condition tags

endometriosisadenomyosis

MeSH descriptors

Cell Movement Endometrium Abortion, Habitual Abortion, Habitual Adenomyosis Adenomyosis Embryo Implantation Embryo Implantation Endometriosis Endometriosis Endometrium Endometrium Female Humans Intercellular Signaling Peptides and Proteins Intercellular Signaling Peptides and Proteins Pregnancy Regeneration Signal Transduction Stem Cells

Citation neighborhood

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.

References (100)

Cited by (40)

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