ArticleEndocrinology2017
Vitamin D Receptor-Dependent Signaling Protects Mice From Dextran Sulfate Sodium-Induced Colitis.
Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- The gut-liver axis modulates intestinal immune homeostasis.Mucosal immunology · 2026Review
- Bile acid receptors regulate the role of intestinal macrophages in inflammatory bowel disease.Frontiers in immunology · 2025Review
- Analysis of 1,25-dihydroxyvitamin D genomic action in human enteroids and colonoids reveals multiple regulatory effects of vitamin D in human intestinal physiology.Frontiers in endocrinology · 2025Article
- Macrophage Metabolic Reprogramming in Inflammatory Bowel Diseases: From Pathogenesis to Therapy.Journal of inflammation research · 2025Review
- Review
- The Impact of Maternal Probiotics on Intestinal Vitamin D Receptor Expression in Early Life.Biomolecules · 2023Article
- Review
- Vitamin D Receptor Mediates Attenuating Effect of Lithocholic Acid on Dextran Sulfate Sodium Induced Colitis in Mice.International journal of molecular sciences · 2023Article
- Article
- Administration ofBioscience of microbiota, food and health · 2023Article
- Vitamin D receptor mediates liver ischemia and reperfusion injury by autophagy-regulated M2 macrophage polarization.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- Monocytic Myeloid-Derived Suppressor Cells from Tumor Tissue Are a Differentiated Cell with Limited Fate Plasticity.ImmunoHorizons · 2022Article
- Vitamin D and Gut Health.Advances in experimental medicine and biology · 2022Article
- The Role of Vitamin D in Immune System and Inflammatory Bowel Disease.Journal of inflammation research · 2022Review
- 1,25-Dihydroxyvitamin DJournal of cellular physiology · 2021Article
- The secondary bile acids, ursodeoxycholic acid and lithocholic acid, protect against intestinal inflammation by inhibition of epithelial apoptosis.Physiological reports · 2020Article
- Arsenic exposure associated T cell proliferation, smoking, and vitamin D in Bangladeshi men and women.PloS one · 2020Observational
- Current evidence for vitamin D in intestinal function and disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Beneficial effects of nutritional supplements on intestinal epithelial barrier functions in experimental colitis modelsWorld journal of gastroenterology · 2019Review
- 1,25-Dihydroxyvitamin D suppresses M1 macrophages and promotes M2 differentiation at bone injury sites.JCI insight · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Low vitamin D status potentiates experimental colitis, but the vitamin D-responsive cell in colitis has not been defined. We hypothesized that vitamin D has distinct roles in colonic epithelial cells and in nonepithelial cells during colitis. We tested this hypothesis by using mice with vitamin D receptor (VDR) deletion from colon epithelial cells (CEC-VDRKO) or nonintestinal epithelial cells (NEC-VDRKO). Eight-week-old mice were treated with 1.35% dextran sulfate sodium (DSS) for 5 days and then euthanized 2 or 10 days after removal of DSS. DSS induced body weight loss and increased disease activity index and spleen size. This response was increased in NEC-VDRKO mice but not CEC-VDRKO mice. DSS-induced colon epithelial damage and immune cell infiltration scores were increased in both mouse models. Although the epithelium healed between 2 and 10 days after DSS administration in control and CEC-VDRKO mice, epithelial damage remained high in NEC-VDRKO mice 10 days after removal of DSS, indicating delayed epithelial healing. Gene expression levels for the proinflammatory, M1 macrophage (Mɸ) cytokines tumor necrosis factor-α, nitric oxide synthase 2, and interleukin-1β were significantly elevated in the colon of NEC-VDRKO mice at day 10. In vitro experiments in murine peritoneal Mɸs demonstrated that 1,25 dihydroxyvitamin D directly inhibited M1 polarization, facilitated M2 polarization, and regulated Mɸ phenotype switching toward the M2 and away from the M1 phenotype. Our data revealed unique protective roles for vitamin D signaling during colitis in the colon epithelium as well as nonepithelial cells in the colon microenvironment (i.e., modulation of Mɸ biology).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.