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Adenomyosis is an oestrogen-dependent gynaecological disease in which a number of factors, such as inflammatory molecules, prostaglandins (PGs), angiogenic factors, cell proliferation and extracellular matrix remodelling proteins, also play a role as key disease mediators. In this study, we used mice lacking both lipocalin and hematopoietic-PG D synthase (L- and H-Pgds) genes in which PGD2 is not produced to elucidate PGD2 roles in the uterus. Gene expression studied by real-time PCR and hormone dosages performed by ELISA or liquid chromatography tandem mass spectroscopy in mouse uterus samples showed that components of the PGD2 signalling pathway, both PGDS and PGD2-receptors, are expressed in the mouse endometrium throughout the oestrus cycle with some differences among uterine compartments. We showed that PGE2 production and the steroidogenic pathway are dysregulated in the absence of PGD2. Histological analysis of L\/H-Pgds\u2212\/\u2212 uteri, and immunohistochemistry and immunofluorescence analyses of proliferation (Ki67), endothelial cell (CD31), epithelial cell (pan-cytokeratin), myofibroblast (\u03b1-SMA) and mesenchymal cell (vimentin) markers, identify that 6-month-old L\/H-Pgds\u2212\/\u2212 animals developed adenomyotic lesions, and that disease severity increased with age. In conclusion, this study suggests that the PGD2 pathway has major roles in the uterus by protecting the endometrium against adenomyosis development. Additional experiments, using for instance transcriptomic approaches, are necessary to fully determine the molecular mechanisms that lead to adenomyosis in L\/H-Pgds\u2212\/\u2212 mice and to confirm whether this strain is an appropriate model for studying the human disease.<\/jats:p>","DOI":"10.1093\/molehr\/gaab029","type":"journal-article","created":{"date-parts":[[2021,4,12]],"date-time":"2021-04-12T13:51:12Z","timestamp":1618235472000},"source":"Crossref","is-referenced-by-count":9,"title":["In the mouse, prostaglandin D2 signalling protects the endometrium against adenomyosis"],"prefix":"10.1093","volume":"27","author":[{"given":"Pascal","family":"Philibert","sequence":"first","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique Humaine, Centre National de la Recherche Scientifique, Universit\u00e9 de Montpellier, Montpellier, France"},{"name":"Laboratoire de Biochimie et Biologie Mol\u00e9culaire, H\u00f4pital Car\u00e8meau, CHU de N\u00eemes, N\u00eemes, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"St\u00e9phanie","family":"D\u00e9jardin","sequence":"additional","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique Humaine, Centre National de la Recherche Scientifique, Universit\u00e9 de Montpellier, Montpellier, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nelly","family":"Pirot","sequence":"additional","affiliation":[{"name":"Institut de Recherche en Canc\u00e9rologie de Montpellier IRCM, Universit\u00e9 de Montpellier, ICM, INSERM, Montpellier, France"},{"name":"BioCampus, RHEM, Universit\u00e9 de Montpellier, CNRS, INSERM, Montpellier, France"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alain","family":"Pruvost","sequence":"additional","affiliation":[{"name":"D\u00e9partement M\u00e9dicaments et Technologies pour la Sant\u00e9 (DMTS), Universit\u00e9 Paris Saclay, CEA, INRAE, SPI, Gif-sur-Yvette, 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