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

The motile and invasive capacity of human endometrial stromal cells: implications for normal and impaired reproductive function
The motile and invasive capacity of human endometrial stromal cells: implications for normal and impaired reproductive function
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
1355-4786
542-557
Weimar, C.H.
1436b5d4-adbe-416f-bd9c-9ea02ba6c6ad
Macklon, N.S.
7db1f4fc-a9f6-431f-a1f2-297bb8c9fb7e
Post Uiterweer, E.D.
f32b08d5-9f36-4917-82f1-a89d1269f377
Brosens, J.J.
35574451-937b-4618-a94c-9509ec9150e1
Gellersen, B.
0c40a571-5956-4d24-837a-19b1eff3d973
Weimar, C.H.
1436b5d4-adbe-416f-bd9c-9ea02ba6c6ad
Macklon, N.S.
7db1f4fc-a9f6-431f-a1f2-297bb8c9fb7e
Post Uiterweer, E.D.
f32b08d5-9f36-4917-82f1-a89d1269f377
Brosens, J.J.
35574451-937b-4618-a94c-9509ec9150e1
Gellersen, B.
0c40a571-5956-4d24-837a-19b1eff3d973

Weimar, C.H., Macklon, N.S., Post Uiterweer, E.D., Brosens, J.J. and Gellersen, B. (2013) The motile and invasive capacity of human endometrial stromal cells: implications for normal and impaired reproductive function. Human Reproduction Update, 19 (5), 542-557. (doi:10.1093/humupd/dmt025). (PMID:23827985)

Record type: Article

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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More information

Published date: July 2013
Organisations: Human Development & Health

Identifiers

Local EPrints ID: 359606
URI: http://eprints.soton.ac.uk/id/eprint/359606
ISSN: 1355-4786
PURE UUID: 8e94cc85-4bd7-4ff9-bcc0-28acc078a95e

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Date deposited: 07 Nov 2013 11:47
Last modified: 22 Jul 2022 18:50

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Contributors

Author: C.H. Weimar
Author: N.S. Macklon
Author: E.D. Post Uiterweer
Author: J.J. Brosens
Author: B. Gellersen

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