The selective vitamin D receptor agonist, elocalcitol, reduces endometriosis development in a mouse model by inhibiting peritoneal inflammation

María Elisa Mariani, Margherita Mariani, Paola Viganò, Davide Gentilini, Barbara Camisa, Elvira Caporizzo, Pietro Di Lucia, Antonella Monno, Massimo Candiani, Edgardo Somigliana, Paola Panina-Bordignon, Paola Panina‐Bordignon
Human Reproduction · 2012 · vol. 27(7) , pp. 2010–2019 · doi:10.1093/humrep/des150 · PMID:22588001 · W2142143935
article OA: bronze CC0 ⤵ 88 in-corpus citations
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The VDR agonist elocalcitol reduced endometriosis development in mice by up to 70% by inhibiting peritoneal inflammation, macrophage recruitment, and cytokine secretion.

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Abstract

BACKGROUND: Endometriosis, which is characterized by the growth of endometrial tissue at ectopic locations as well as vascular development and inflammation, is still an unmet clinical need since an optimal drug that allows for both pain and infertility management does not exist. Since both the eutopic and the ectopic endometrium express the vitamin D receptor (VDR), and VDR agonists are endowed with anti-proliferative and anti-inflammatory properties, we evaluated the effect of elocalcitol, a VDR agonist with low calcaemic liability, in a mouse model of experimentally induced endometriosis. METHODS AND RESULTS: Endometriosis was induced by injection of syngeneic endometrial tissue fragments into adult Balb/c female mice. After having confirmed by immunohistochemistry that endometriotic lesions developing in mice expressed VDR, the mice were administered with elocalcitol (100 μg/kg) or vehicle orally, once a day, for various durations of time. In this model, elocalcitol was able to reduce total lesion weight up to 70% upon treatment for 1 week before and 2 weeks after disease induction. Interestingly, a therapeutic effect was also observed on already established lesions. Elocalcitol was shown to reduce the capacity of mouse endometrial cells to adhere to collagen. In addition in treated mice, a decreased state of peritoneal inflammation was demonstrated by the inhibition of macrophage recruitment and inflammatory cytokine secretion. CONCLUSIONS: The VDR agonist elocalcitol inhibits lesion development in a validated mouse model of endometriosis, and exerts a protective effect on both the implantation and organization of transferred endometrial tissue. These preliminary data in mice provide a sound rationale for further testing in primate models and eventually in humans.

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Condition tags

endometriosisinfertility

MeSH descriptors

Calcitriol Endometriosis Inflammation Peritoneum Receptors, Calcitriol Animals Calcitriol Calcitriol Cell Adhesion Cell Proliferation Cytokines Cytokines Disease Models, Animal Endometriosis Female Gonadotropin-Releasing Hormone Gonadotropin-Releasing Hormone Humans Inflammation Macrophages, Peritoneal

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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