Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis
Endometriosis is a debilitating disease affecting 190 million women worldwide and the greatest single contributor to infertility. The most broadly accepted etiology is that uterine endometrial cells retrogradely enter the peritoneum during menses, and implant and form invasive lesions in a process a...
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eLife Sciences Publications Ltd
2024-12-01
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| Online Access: | https://elifesciences.org/articles/94778 |
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| author | Chun-Wei Chen Jeffery B Chavez Ritikaa Kumar Virginia Arlene Go Ahvani Pant Anushka Jain Srikanth R Polusani Matthew J Hart Randal D Robinson Maria Gaczynska Pawel Osmulski Nameer B Kirma Bruce J Nicholson |
| author_facet | Chun-Wei Chen Jeffery B Chavez Ritikaa Kumar Virginia Arlene Go Ahvani Pant Anushka Jain Srikanth R Polusani Matthew J Hart Randal D Robinson Maria Gaczynska Pawel Osmulski Nameer B Kirma Bruce J Nicholson |
| author_sort | Chun-Wei Chen |
| collection | DOAJ |
| description | Endometriosis is a debilitating disease affecting 190 million women worldwide and the greatest single contributor to infertility. The most broadly accepted etiology is that uterine endometrial cells retrogradely enter the peritoneum during menses, and implant and form invasive lesions in a process analogous to cancer metastasis. However, over 90% of women suffer retrograde menstruation, but only 10% develop endometriosis, and debate continues as to whether the underlying defect is endometrial or peritoneal. Processes implicated in invasion include: enhanced motility; adhesion to, and formation of gap junctions with, the target tissue. Endometrial stromal (ESCs) from 22 endometriosis patients at different disease stages show much greater invasiveness across mesothelial (or endothelial) monolayers than ESCs from 22 control subjects, which is further enhanced by the presence of EECs. This is due to the enhanced responsiveness of endometriosis ESCs to the mesothelium, which induces migration and gap junction coupling. ESC-PMC gap junction coupling is shown to be required for invasion, while coupling between PMCs enhances mesothelial barrier breakdown. |
| format | Article |
| id | doaj-art-517fc9d29ef640179cfd969605607c24 |
| institution | Kabale University |
| issn | 2050-084X |
| language | English |
| publishDate | 2024-12-01 |
| publisher | eLife Sciences Publications Ltd |
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| series | eLife |
| spelling | doaj-art-517fc9d29ef640179cfd969605607c242025-01-13T16:27:25ZengeLife Sciences Publications LtdeLife2050-084X2024-12-011310.7554/eLife.94778Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosisChun-Wei Chen0https://orcid.org/0000-0002-3318-0349Jeffery B Chavez1Ritikaa Kumar2Virginia Arlene Go3Ahvani Pant4Anushka Jain5Srikanth R Polusani6Matthew J Hart7Randal D Robinson8Maria Gaczynska9Pawel Osmulski10Nameer B Kirma11https://orcid.org/0000-0002-4657-3774Bruce J Nicholson12https://orcid.org/0000-0003-1649-7173Department of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesDepartment of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesDepartment of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesDepartment of Obstetrics and Gynecology, UT Health San Antonio, San Antonio, United StatesDepartment of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesDepartment of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesDepartment of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesCenter for Innovative Drug Discovery, UT Health San Antonio, San Antonio, United StatesDepartment of Obstetrics and Gynecology, UT Health San Antonio, San Antonio, United StatesDepartment of Molecular Medicine, UT Health San Antonio, San Antonio, United StatesDepartment of Molecular Medicine, UT Health San Antonio, San Antonio, United StatesDepartment of Molecular Medicine, UT Health San Antonio, San Antonio, United StatesDepartment of Biochemistry and Structural Biology, UT Health San Antonio, San Antonio, United StatesEndometriosis is a debilitating disease affecting 190 million women worldwide and the greatest single contributor to infertility. The most broadly accepted etiology is that uterine endometrial cells retrogradely enter the peritoneum during menses, and implant and form invasive lesions in a process analogous to cancer metastasis. However, over 90% of women suffer retrograde menstruation, but only 10% develop endometriosis, and debate continues as to whether the underlying defect is endometrial or peritoneal. Processes implicated in invasion include: enhanced motility; adhesion to, and formation of gap junctions with, the target tissue. Endometrial stromal (ESCs) from 22 endometriosis patients at different disease stages show much greater invasiveness across mesothelial (or endothelial) monolayers than ESCs from 22 control subjects, which is further enhanced by the presence of EECs. This is due to the enhanced responsiveness of endometriosis ESCs to the mesothelium, which induces migration and gap junction coupling. ESC-PMC gap junction coupling is shown to be required for invasion, while coupling between PMCs enhances mesothelial barrier breakdown.https://elifesciences.org/articles/94778gap junctionsinvasionendometriosismotility |
| spellingShingle | Chun-Wei Chen Jeffery B Chavez Ritikaa Kumar Virginia Arlene Go Ahvani Pant Anushka Jain Srikanth R Polusani Matthew J Hart Randal D Robinson Maria Gaczynska Pawel Osmulski Nameer B Kirma Bruce J Nicholson Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis eLife gap junctions invasion endometriosis motility |
| title | Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis |
| title_full | Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis |
| title_fullStr | Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis |
| title_full_unstemmed | Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis |
| title_short | Hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis |
| title_sort | hypersensitive intercellular responses of endometrial stromal cells drive invasion in endometriosis |
| topic | gap junctions invasion endometriosis motility |
| url | https://elifesciences.org/articles/94778 |
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