Commentary: Somatic Stem Cells and Their Dysfunction in Endometriosis

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This commentary discusses the role of somatic stem cell dysfunction in the pathogenesis of endometriosis, exploring potential therapeutic targets for disease management.

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This commentary reviews somatic stem cells—particularly endometrial stem cells—and how their dysfunction may contribute to endometriosis pathogenesis, discussing high-level mechanisms such as EMT/MET, stem cell niches, menstrual-effluent–induced signaling, and the potential contribution of bone marrow–derived stem cells. The authors highlight evidence that EMT/MET-like processes and EMT activity in side population cells could facilitate migration, invasion, and ectopic lesion establishment, and they cite studies linking miR-200b and ZEB1/2/KLF4 to EMT, invasiveness, and stemness. A key limitation is that the piece is a narrative commentary compiling findings from multiple studies rather than presenting new experimental data, and it frames many connections as associations requiring further investigation. This paper is centrally about endometriosis — it synthesizes literature on somatic/endometrial stem cells and their dysregulation in relation to EMT/MET and the stem-cell niche in endometriosis.

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Abstract

GENERAL COMMENTARY article Front. Surg., 14 July 2017Sec. Obstetrics and Gynecological Surgery Volume 4 - 2017 | https://doi.org/10.3389/fsurg.2017.00037
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References

1 DjokovicDCalhaz-JorgeC. Somatic stem cells and their dysfunction in endometriosis. Front Surg (2015) 1:51.10.3389/fsurg.2014.00051 2 VerdiJTanAShoae-HassaniASeifalianAM. Endometrial stem cells in regenerative medicine. J Biol Eng (2014) 8:20.10.1186/1754-1611-8-20 3 MirantesCEspinosaIFerrerIDolcetXPratJMatias-GuiuX. Epithelial-to-mesenchymal transition and stem cells in endometrial cancer. Hum Pathol (2013) 44(10):1973–81.10.1016/j.humpath.2013.04.009 4 MatsuzakiSDarchaC. Epithelial to mesenchymal transition-like and mesenchymal to epithelial transition-like processes might be involved in the pathogenesis of pelvic endometriosis. Hum Reprod (2012) 27(3):712–21.10.1093/humrep/der442 5 DemirAYDemolHPuypeMde GoeijAFDunselmanGAHerrlerAet alProteome analysis of human mesothelial cells during epithelial to mesenchymal transitions induced by shed menstrual effluent. Proteomics (2004) 4(9):2608–23.10.1002/pmic.200300827 6 BarraganFIrwinJCBalayanSEriksonDWChenJCHoushdaranSet alHuman endometrial fibroblasts derived from mesenchymal progenitors inherit progesterone resistance and acquire an inflammatory phenotype in the endometrial niche in endometriosis. Biol Reprod (2016) 94(5):118.10.1095/biolreprod.115.136010 7 EggersJCMartinoVReinboldRSchäferSDKieselLStarzinski-PowitzAet almicroRNA miR-200b affects proliferation, invasiveness and stemness of endometriotic cells by targeting ZEB1, ZEB2 and KLF4. Reprod Biomed Online (2016) 32(4):434–45.10.1016/j.rbmo.2015.12.013 8 DuHTaylorHS. Contribution of bone marrow-derived stem cells to endometrium and endometriosis. Stem Cells (2007) 25(8):2082–6.10.1634/stemcells.2006-0828 9 OliveDLPrittsEA. Treatment of endometriosis. N Engl J Med (2001) 345:266–75.10.1056/NEJM200107263450407 10 WangXMamillapalliRMutluLDuHTaylorHS. Chemoattraction of bone marrow-derived stem cells towards human endometrial stromal cells is mediated by estradiol regulated CXCL12 and CXCR4 expression. Stem Cell Res (2015) 15(1):14–22.10.1016/j.scr.2015.04.004 Summary

Keywords

somatic stem cells, endometriosis, mesenchymal to epithelial transition, epithelial to mesenchymal transition, stem cell niche Citation Tampaki EC, Tampakis A, Kontzoglou K and Kouraklis G (2017) Commentary: Somatic Stem Cells and Their Dysfunction in Endometriosis. Front. Surg. 4:37. doi: 10.3389/fsurg.2017.00037 Received 06 April 2017 Accepted 29 June 2017 Published 14 July 2017 Volume 4 - 2017 Edited by Christine Wyns, Université catholique de Louvain, Belgium Reviewed by Salim Alfred Bassil, Al Arz Hospital, Lebanon Updates Copyright © 2017 Tampaki, Tampakis, Kontzoglou and Kouraklis. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. *Correspondence: Ekaterini Christina Tampaki, [email protected] Specialty section: This article was submitted to Obstetrics and Gynecology, a section of the journal Frontiers in Surgery Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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endometriosis

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