RSS-Feed abonnieren
DOI: 10.1055/a-1894-6817
Genes Relating to Biological Processes of Endometriosis: Expression Changes Common to a Mouse Model and Patients
![](https://www.thieme-connect.de/media/drugres/202209/lookinside/thumbnails/2022-06-2537_10-1055-a-1894-6817-1.jpg)
Abstract
Endometriosis is one of the most common gynecological diseases in women of reproductive age. Retrograde menstruation is considered a major reason for the development of endometriosis. The syngeneic transplantation mouse model is an endometriosis animal model that is considered to mimic retrograde menstruation. However, it remains poorly understood which genetic signatures of endometriosis are reflected in this model. Here, we employed an in vivo syngeneic mouse endometriosis model and identified differentially expressed genes (DEGs) between the ectopic and eutopic tissues using microarray analysis. Three gene expression profile datasets, GSE5108, GSE7305, and GSE11691, were downloaded from the Gene Expression Omnibus database and DEGs between ectopic and eutopic tissues from the same patients were identified. Gene ontology analysis of the DEGs revealed that biological processes including cell adhesion, the inflammatory response, the response to mechanical stimulus, cell proliferation, and extracellular matrix organization were enriched in both the model and patients. Of the 195 DEGs common to the model and patients, 154 showed the same expression pattern, and 28 of these 154 DEGs came up when PubMed was searched for each gene along with the terms “endometriosis” and “development”. This is the first comparison of the DEGs of the mouse syngeneic endometriosis model and those of patients, and we identified the biological processes common to the model and patients at the transcriptional level. This model may be useful to evaluate the efficacy of drugs which target these biological processes.
Key words
endometriosis - mouse syngeneic model - DNA microarray - patients - differentially expressed genes - biological processPublikationsverlauf
Eingereicht: 06. Januar 2022
Angenommen: 05. Juli 2022
Artikel online veröffentlicht:
02. September 2022
© 2022. Thieme. All rights reserved.
Georg Thieme Verlag
Rüdigerstraße 14, 70469 Stuttgart,
Germany
-
References
- 1 Giudice LC. Endometriosis. Clinical Practice. N Engl J Med 2010; 362: 2389-2398
- 2 Nnoaham KE, Hummelshoj L, Webster P. et al. World Endometriosis Research Foundation Global Study of Women's Health Consortium. Impact of endometriosis on quality of life and work productivity: a multicenter study across ten countries. Fertil Steril 2011; 96: 366-373
- 3 Kalaitzopoulos DR, Samartzis N, Kolovos GN. et al. Treatment of endometriosis: a review with comparison of 8 guidelines. BMC Women’s Health 2021; 21: 397
- 4 Donnez J, Dolmans MM. Endometriosis and medical therapy: from progestogens to progesterone resistance to GnRH antagonists: a review. J Clin Med 2021; 10: 1085
- 5 Laganà AS, Garzon S, Franchi M. et al. Translational animal models for endometriosis research: a long and windy road. Ann Transl Med 2018; Nov 6: 431
- 6 Burns KA, Rodriguez KF, Hewitt SC. et al. Role of estrogen receptor signaling required for endometriosis-like lesion establishment in a mouse model. Endocrinology. 2012; 153: 3960-39671
- 7 Sampson JA. Peritoneal endometriosis due to the menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 1927; 14: 422-469
- 8 Goulielmos GN, Matalliotakis M, Matalliotaki C. et al. Endometriosis research in the -omics era. Gene. 2020; 741: 144545
- 9 Huang DW, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID Bioinformatics Resources. Nat Protoc 2009; 4: 44-57
- 10 Kupershmidt I, Su QJ, Grewal A. et al. Ontology-based meta-analysis of global collections of high-throughput public data. PLoS One 2010; 5: e13066
- 11 Eyster KM, Klinkova O, Kennedy V. et al. Whole genome deoxyribonucleic acid microarray analysis of gene expression in ectopic versus eutopic endometrium. Fertil Steril 2007; 88: 1505-1533
- 12 Hever A, Roth RB, Hevezi P. et al. Human endometriosis is associated with plasma cells and overexpression of B lymphocyte stimulator. Proc Nat Acad Sci U S A. 2007; 104: 12451-12456
- 13 Hull ML, Escareno CR, Godsland JM. et al. Endometrial-peritoneal interactions during endometriotic lesion establishment. Am J Pathol 2008; 173: 700-715
- 14 Ramón LA, Braza-Boïls A, Gilabert-Estellés J. et al. microRNAs expression in endometriosis and their relation to angiogenic factors. Hum Reprod 2011; 26: 1082-1090
- 15 Luddi A, Marrocco C, Governini L. et al. Expression of matrix metalloproteinases and their inhibitors in endometrium: high levels in endometriotic lesions. Int J Mol Sci 2020; 21: 2840
- 16 Liu T, Liu M, Zheng C. et al. Exosomal lncRNA CHL1-AS1 derived from peritoneal macrophages promotes the progression of endometriosis via the miR-610/MDM2 axis. Int J Nanomedicine 2021; 16: 5451-5464
- 17 Ma J, Zhang L, Zhan H. et al. Single-cell transcriptomic analysis of endometriosis provides insights into fibroblast fates and immune cell heterogeneity. Cell Biosci 2021; 11: 125
- 18 Zhong Q, Yang F, Chen X. et al. Patterns of Immune Infiltration in Endometriosis and Their Relationship to r-AFS Stages. Front Genet 2021; 12: 631715
- 19 Shao R, Cao S, Wang X. et al. The elusive and controversial roles of estrogen and progesterone receptors in human endometriosis. Am J Transl Res 2014; 6: 104-113
- 20 Khan KN, Kitajima M, Hiraki K. et al. Escherichia coli contamination of menstrual blood and effect of bacterial endotoxin on endometriosis. Fertil Steril 2010; 94: 2860-2863
- 21 Greaves E, Critchley HOD, Horne AW. et al. Relevant human tissue resources and laboratory models for use in endometriosis research. Acta Obstet Gynecol Scand 2017; 96: 644-658
- 22 Mishra A, Galvankar M, Vaidya S. et al. Mouse model for endometriosis is characterized by proliferation and inflammation but not epithelial-to-mesenchymal transition and fibrosis. J Biosci 2020; 45: 105