Cyr61, a deregulated gene in endometriosis
Abstract
Gene expression profiling was performed to identify genes involved in the development of endometriosis. In the secretory phase of the menstrual cycle, several estrogen-regulated genes were up-regulated in endometria of women with endometriosis. The most consistent regulation with one of the highest factors was observed for the Cyr61 gene, which codes for a secreted, cysteine-rich, heparin-binding protein that promotes cell adhesion, migration, and neovascularization. Estrogen responsiveness of endometrial Cyr61 expression was suggested by the higher expression during the proliferative phase and the reduction observed in human endometrial fragments grafted into nude mice subsequently treated with an anti-estrogen. The expression level of Cyr61 was found to be further increased in ectopic endometriotic lesions, as compared to eutopic endometria. In these lesions, an imbalance in expression of the estrogen-converting enzymes 17beta-hydroxysteroid dehydrogenase type 1 and 2 was found, which might explain the elevated Cyr61 level. However, Cyr61 expression was not altered in endometriotic lesions of women treated with a GnRH agonist. These results suggest that Cyr61 may represent a gene characteristic for endometriosis and also play an important role in the development and persistence of endometriotic lesions.
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Significant differences in gene expression exist in eutopic endometrium from women with versus without endometriosis at the transcript level.
“At the transcript level, significant differences in gene expression exist in eutopic endometrium from women with versus without endometriosis [114–117].”
From Update on biomarkers for the detection of endometriosis (2015) · cites this paper as [114]
Cyr61 is up-regulated in eutopic endometrium in women with endometriosis and also in ectopic lesions as well as in experimental endometriosis.
“A highly estrogen-dependent gene, Cyr61, is up-regulated in eutopic endometrium in women with endometriosis and also in ectopic lesions as well as in experimental endometriosis [42, 43].”
From The pathophysiology of endometriosis and adenomyosis, tissue injury and repair (2009) · cites this paper as [42]
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- Authors
- Absenger, Y.
- Affiliations
- Essen University Hospital (DE)
- Corresponding author
- Absenger, Y.
- Venue
- Molecular Human Reproduction
- Publisher
- Oxford University Press (OUP)
- Published
- 2004-03-25
- Volume
- 10
- Issue
- 6
- Pages
- 399-407
- ISSN
- 1360-9947 (ISSN-L)
- 1460-2407
- OpenAlex
- W2127850483
- Cited by
- 95
- References
- 46
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 3 · 2018: 5 · 2017: 3 · 2016: 4 · 2015: 4 · 2014: 4 · 2013: 2 · 2012: 5
- FWCI
- 7.14
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Human Reproduction (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Universität Duisburg-Essen
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ectopic Pregnancy Diagnosis and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- CYR61, endometriosis, endometrium, estrogen regulation, menstrual cycle, luteal phase, proliferative phase, 17β-hydroxysteroid dehydrogenase, antiestrogens, GnRH agonist, heparin-binding protein, gene expression profiling
- MeSH terms
- Adult, Animals, Aromatase, Endometriosis, Endometrium, Estrogens, Female, Gene Expression Regulation, Humans, Gonadotropin-Releasing Hormone, Menstrual Cycle, Mice, Nude, Middle Aged, Transplantation, Heterologous, 17-Hydroxysteroid Dehydrogenases, Tissue Transplantation, Immediate-Early Proteins, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Intercellular Signaling Peptides and Proteins, Angiogenesis Inducing Agents, Mice, Cysteine-Rich Protein 61
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