Abstract
The vitamin D receptor (VDR) and aryl hydrocarbon receptor (AHR) are two nuclear receptors that exert their effects by binding with ligands and forming a molecular complex. These complexes translocate to the nucleus and activate the expression of a series of genes which have a response element to VDR or AHR. Both receptors have been identified in the pathogenesis of endometriosis, a common disease characterized by the formation of endometrium-like tissue in ectopic zones. Despite numerous therapies, there is no definitive cure for endometriosis at the pharmacological level. Our study aims to describe the location and the expression of VDR and AHR at the protein level. For this purpose, an evaluation was performed using tissue from the three normal phases of the endometrium (proliferative, early, and late secretory) and in endometriosis by immunohistochemistry, using anti-VDR and anti-AHR antibodies. We demonstrate that in the nuclei of glandular cells in endometriosis, the expression of VDR and AHR is mutually exclusive—when the expression of one receptor is high, the other one is low—suggesting a possible target in the treatment of endometriosis. We also identify a significant change in the expression of glandular cytoplasmic AHR between the proliferative and late secretory endometrium.
Highlights
The vitamin D receptor (VDR) and aryl hydrocarbon receptor (AHR) are two nuclear receptors which have been associated with endometriosis (Sayegh et al 2014; Rier et al 1993)
The endometrium is a very differentiated tissue, and the expression of VDR may contribute to the pathogenesis of endometriosis in terms of induction of endometrial-like differentiation in tissue where endometrial cells should not be present
Our data show an upregulation of AHR in proliferative endometrium compared to late secretory endometrium, which is consistent with a proliferation activity of AHR in the endometrium
Summary
The vitamin D receptor (VDR) and aryl hydrocarbon receptor (AHR) are two nuclear receptors which have been associated with endometriosis (Sayegh et al 2014; Rier et al 1993). The disorder is defined as the growth of endometrial tissue outside the cavum uteri, and it is postulated to invoke a chronic inflammatory reaction (Agic et al 2007). Endometriosis shares several similarities with malignant diseases, such as reduced apoptosis, invasion of endometrial cells into adjacent organs (bowel, bladder), increased angiogenesis (Varma et al 2004), and recurrence (Donnez et al 2002). Vitamin D and its receptor (VDR) regulate numerous physiological and pharmaceutical processes, including bone and calcium metabolism, cellular growth and differentiation, immunity, and cardiovascular functions (Nagpal et al 2005; Choi and Makishima 2009). Numerous in vitro and in vivo studies have shown that vitamin D is a potent inhibitor of cellular proliferation in a wide range of cell
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