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      A simple and sensitive method to detect vitamin D receptor expression in various disease models using stool samples

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          Abstract

          Vitamin D receptor (VDR) executes the main biological functions of its ligand vitamin D. VDR/vitamin D plays critical roles in regulating host immunity, maintaining barrier functions, and shaping gut microbiome. Reduction of intestinal VDR has been reported in various diseases, including inflammatory diseases and colon cancer. However, it is always challenging to get biopsies to test the pathologic changes of VDR in intestine. In the current study, we reported a simple and sensitive quantitative PCR (qPCR) method to detect reduction of intestinal VDR using fecal samples. We validated this method in several experimental models, such as colitis, bacterial infection, and aging. We further correlated the qPCR data of VDR with the protein level of VDR in colon or serum 25 (OH)D 3 in mice with different VDR status (VDR +/+, VDR +/-, and VDR −/−). Our data indicate that the qPCR method to test VDR using fecal samples could detect the expression level of intestinal VDR in various diseases. Our study highlights the feasibility, sensitivity, and simplicity of a molecular method to study the status of VDR as a biomarker.

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          Most cited references23

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          Exploring vitamin D metabolism and function in cancer

          Vitamin D, traditionally known as an essential nutrient, is a precursor of a potent steroid hormone that regulates a broad spectrum of physiological processes. In addition to its classical roles in bone metabolism, epidemiological, preclinical, and cellular research during the last decades, it revealed that vitamin D may play a key role in the prevention and treatment of many extra-skeletal diseases such as cancer. Vitamin D, as a prohormone, undergoes two-step metabolism in liver and kidney to produce a biologically active metabolite, calcitriol, which binds to the vitamin D receptor (VDR) for the regulation of expression of diverse genes. In addition, recent studies have revealed that vitamin D can also be metabolized and activated through a CYP11A1-driven non-canonical metabolic pathway. Numerous anticancer properties of vitamin D have been proposed, with diverse effects on cancer development and progression. However, accumulating data suggest that the metabolism and functions of vitamin D are dysregulated in many types of cancer, conferring resistance to the antitumorigenic effects of vitamin D and thereby contributing to the development and progression of cancer. Thus, understanding dysregulated vitamin D metabolism and function in cancer will be critical for the development of promising new strategies for successful vitamin D-based cancer therapy.
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            Intestinal epithelial vitamin D receptor deletion leads to defective autophagy in colitis.

            Vitamin D and the vitamin D receptor (VDR) appear to be important immunological regulators of inflammatory bowel diseases (IBD). Defective autophagy has also been implicated in IBD, where interestingly, polymorphisms of genes such as ATG16L1 have been associated with increased risk. Although vitamin D, the microbiome and autophagy are all involved in pathogenesis of IBD, it remains unclear whether these processes are related or function independently.
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              Intestinal epithelial vitamin D receptor signaling inhibits experimental colitis.

              The inhibitory effects of vitamin D on colitis have been previously documented. Global vitamin D receptor (VDR) deletion exaggerates colitis, but the relative anticolitic contribution of epithelial and nonepithelial VDR signaling is unknown. Here, we showed that colonic epithelial VDR expression was substantially reduced in patients with Crohn's disease or ulcerative colitis. Moreover, targeted expression of human VDR (hVDR) in intestinal epithelial cells (IECs) protected mice from developing colitis. In experimental colitis models induced by 2,4,6-trinitrobenzenesulfonic acid, dextran sulfate sodium, or CD4(+)CD45RB(hi) T cell transfer, transgenic mice expressing hVDR in IECs were highly resistant to colitis, as manifested by marked reductions in clinical colitis scores, colonic histological damage, and colonic inflammation compared with WT mice. Reconstitution of Vdr-deficient IECs with the hVDR transgene completely rescued Vdr-null mice from severe colitis and death, even though the mice still maintained a hyperresponsive Vdr-deficient immune system. Mechanistically, VDR signaling attenuated PUMA induction in IECs by blocking NF-κB activation, leading to a reduction in IEC apoptosis. Together, these results demonstrate that gut epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this anticolitic activity is independent of nonepithelial immune VDR actions.
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                Author and article information

                Contributors
                Journal
                Genes Dis
                Genes Dis
                Genes & Diseases
                Chongqing Medical University
                2352-4820
                2352-3042
                17 March 2020
                November 2021
                17 March 2020
                : 8
                : 6
                : 939-945
                Affiliations
                [a ]Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, Chicago, IL 60612, USA
                [b ]UIC Cancer Center, University of Illinois at Chicago, Chicago, IL 60612, USA
                [c ]Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL 60612, USA
                Author notes
                []Corresponding author. Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, 840 S Wood Street, Room 704 CSB, MC716, Chicago, IL 60612, USA. junsun7@ 123456uic.edu
                Article
                S2352-3042(20)30044-1
                10.1016/j.gendis.2020.03.002
                8427243
                34522720
                ea13dcfe-60f7-4fce-8bd5-7e7903ddc094
                © 2020 Chongqing Medical University. Production and hosting by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 8 January 2020
                : 24 February 2020
                : 6 March 2020
                Categories
                Article

                aging,biomarker,correlation,infection,inflammation,microbiome,salmonella,vitamin d deficiency

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