Reactive Oxygen Species Controls Endometriosis Progression
Open accessAbstract
Endometriosis is associated with chronic inflammation, and reactive oxygen species (ROS) are proinflammatory mediators that modulate cell proliferation. We have investigated whether the dysregulation of ROS production in endometriotic cells correlates with a pro-proliferative phenotype and can explain the spreading of this disease. Stromal and epithelial cells were purified from ovarian endometrioma and eutopic endometrium from 14 patients with endometriosis to produce four primary cell lines from each patient. ROS production, detoxification pathways, cell proliferation, and mitogen-activated protein kinase pathway activation were studied and compared with epithelial and stromal cell lines from 14 patients without endometriosis. Modulation of the proliferation of endometriosis by N-acetyl-cysteine, danazol, and mifepristone was tested in vitro and in 28 nude mice implanted with endometriotic tissue of human origin. Endometriotic cells displayed higher endogenous oxidative stress with an increase in ROS production, alterations in ROS detoxification pathways, and a drop in catalase levels, as observed for tumor cells. This increase in endogenous ROS correlated with increased cellular proliferation and activation of ERK1/2. These phenomena were abrogated by the antioxidant molecule N-acetyl-cysteine both in vitro and in a mouse model of endometriosis. Human endometriotic cells display activated pERK, enhanced ROS production, and proliferative capability. Our murine model shows that antioxidant molecules could be used as safe and efficient treatments for endometriosis.
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These results suggest that antioxidant molecules could potentially be used as a treatment option for endometriosis.
“These results suggest that antioxidant molecules could potentially be used as a treatment option for endometriosis.75”
From Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France (2013) · cites this paper as [75]
The increase in endogenous ROS in endometriotic cells correlated with increased cellular proliferation and activation of ERK1/2.
“This increase in endogenous ROS correlated with increased cellular proliferation and activation of ERK1/2.”
From Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France (2013) · cites this paper as [75]
Endometriotic cells display higher endogenous oxidative stress with an increase in ROS production, alterations in ROS detoxification pathways, and a drop in catalase levels.
“Endometriotic cells display higher endogenous oxidative stress with an increase in ROS production, alterations in ROS detoxification pathways, and a drop in catalase levels.”
From Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France (2013) · cites this paper as [75]
N-acetyl-cysteine abrogated these phenomena both in vitro and in a mouse model of endometriosis.
“These phenomena were abrogated by the antioxidant molecule N-acetyl-cysteine both in vitro and in a mouse model of endometriosis.”
From Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France (2013) · cites this paper as [75]
Dysregulation of ROS production in endometriotic cells correlates with a proproliferative phenotype and may be implicated in the spreading of the disease.
“The dysregulation of ROS production in endometriotic cells correlates with a proproliferative phenotype and may be implicated in the spreading of the disease.75”
From Defining Future Directions for Endometriosis Research: Workshop Report From the 2011 World Congress of Endometriosis in Montpellier, France (2013) · cites this paper as [75]
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Self-citation
- Authors
- Ngô, C., Chéreau, C., Nicco, C., Weill, B., Chapron, C., & Batteux, F.
- Affiliations
- Hôpital Cochin (FR)
- Corresponding author
- Batteux, Frédéric
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 175
- Issue
- 1
- Pages
- 225-234
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC2708809
- OpenAlex
- W2006808109
- Cited by
- 292
- References
- 39
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 15 · 2023: 24 · 2022: 20 · 2021: 23 · 2020: 18 · 2019: 13 · 2018: 16 · 2017: 15 · 2016: 14 · 2015: 18 · 2014: 17 · 2013: 20 · 2012: 21
- FWCI
- 18.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Keywords
- endometriosis, reactive oxygen species, oxidative stress, endometrioma, endometrial stromal cells, endometrial epithelial cells, cell proliferation, ERK1/2 activation, MAPK signaling, catalase, N-acetylcysteine, antioxidants, danazol, mifepristone, chronic inflammation, xenograft mouse model
- MeSH terms
- Adult, Animals, Antioxidants, Catalase, Cell Line, Endometriosis, Female, Humans, Hydrogen Peroxide, Mice, Nude, Superoxide Dismutase, Blotting, Western, Reactive Oxygen Species, Oxidative Stress, Disease Progression, Extracellular Signal-Regulated MAP Kinases, Cell Proliferation, Mice
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