Vitamin D3 induces vitamin D receptor and HDAC11 binding to relieve the promoter of the tight junction proteins

Li, Fenghua; Li, Shanshan; Li, Xiaoxi; Wang, Shuai; Li, Mao-Gang; Guan, Li; Luan, Tiangang; Liu, Zhigang; Liu, Zhanju; Yang, Ping‐Chang

doi:10.18632/oncotarget.17692

Cited by 26 publications

(21 citation statements)

References 28 publications

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“…These results suggested that claudins have different biology function in the different cells or tissues. In our study, other TJ molecules such as ZO-1 and occludin were significantly reduced in VDR -/mice, suggesting that chronic inflammation induced by VDR deletion may affect the barrier function of TJs and may correlate with the interaction between VDR and histone deacetylase 11 (HDAC11) 39 .…”

Section: Claudin-10mentioning

confidence: 50%

Vitamin D Receptor Deletion Leads to the Destruction of Tight and Adherens Junctions in Lungs

et al. 2018

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Vitamin D deficiency has been linked to various inflammatory diseases in lungs, including pneumonia, asthma and chronic obstructive pulmonary disease. However, the mechanisms by which vitamin D and vitamin D receptor reduce inflammation in lung diseases remain poorly understood. In this study, we investigated the expression and cell-specific distribution of tight and adherens junctions in the lungs of vitamin D receptor-deficient (VDR -/-) mice. Our results demonstrated that mRNA and protein levels of claudin-2, claudin-4 and claudin-12 were significantly decreased in the lungs of VDR -/mice. Other tight and adherens junction proteins, such as ZO-1, occludin, claudin-10, β-catenin, and VE-cadherin, showed significant differences in expression in the lungs of VDR -/and wild-type mice. These data suggest that altered expression of tight and adherens junction molecules, especially of claudin-2, −4, −10, −12, and −18, after chronic pneumonia caused by VDR deletion could increase lung permeability.Therefore, VDR may play an important role in maintaining pulmonary barrier integrity. Further studies should confirm whether vitamin D/VDR is beneficial for the prevention or treatment of lung diseases. ARTICLE HISTORY

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Section: Claudin-10mentioning

confidence: 50%

Vitamin D Receptor Deletion Leads to the Destruction of Tight and Adherens Junctions in Lungs

et al. 2018

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“…Although there is a variety of functions and routes that vitamin D/VDR plays a role, there are few studies exploring gene regulation of junctional proteins [ 117 ]. Liu et al showed that VDR binds to histone inhibiting transcription of ZO-1, claudin-5, and occludin genes [ 118 ]. Zhang et al have identified that VDR increases the tight junction protein claudin-2 as a direct target of the VDR signaling pathway [ 62 ].…”

Section: Epigenetics and Ibdmentioning

confidence: 99%

Vitamin D Modulates Intestinal Microbiota in Inflammatory Bowel Diseases

Battistini

Ballan

Herkenhoff

et al. 2020

IJMS

103

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Inflammatory bowel disease (IBD) is a chronic inflammation of the gastrointestinal tract (GIT), including Crohn’s disease (CD) and ulcerative colitis (UC), which differ in the location and lesion extensions. Both diseases are associated with microbiota dysbiosis, with a reduced population of butyrate-producing species, abnormal inflammatory response, and micronutrient deficiency (e.g., vitamin D hypovitaminosis). Vitamin D (VitD) is involved in immune cell differentiation, gut microbiota modulation, gene transcription, and barrier integrity. Vitamin D receptor (VDR) regulates the biological actions of the active VitD (1α,25-dihydroxyvitamin D3), and is involved in the genetic, environmental, immune, and microbial aspects of IBD. VitD deficiency is correlated with disease activity and its administration targeting a concentration of 30 ng/mL may have the potential to reduce disease activity. Moreover, VDR regulates functions of T cells and Paneth cells and modulates release of antimicrobial peptides in gut microbiota-host interactions. Meanwhile, beneficial microbial metabolites, e.g., butyrate, upregulate the VDR signaling. In this review, we summarize the clinical progress and mechanism studies on VitD/VDR related to gut microbiota modulation in IBD. We also discuss epigenetics in IBD and the probiotic regulation of VDR. Furthermore, we discuss the existing challenges and future directions. There is a lack of well-designed clinical trials exploring the appropriate dose and the influence of gender, age, ethnicity, genetics, microbiome, and metabolic disorders in IBD subtypes. To move forward, we need well-designed therapeutic studies to examine whether enhanced vitamin D will restore functions of VDR and microbiome in inhibiting chronic inflammation.

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“…103 Curcumin is taken up by the intestinal epithelial cells 104 and Bartik et al showed that curcumin binds to intracellular vitamin D receptor in intestinal epithelial cells and facilitates colon cancer chemoprevention. 105 It needs to be emphasized that interaction between vitamin D and HDAC is associated with the regulation of epithelial barrier functions 106 and it is likely that by enhancing vitamin D signaling, curcumin regulates barrier function.…”

Section: Other Intestine-specific Effects Of Curcuminmentioning

confidence: 99%

Curcumin-mediated regulation of intestinal barrier function: The mechanism underlying its beneficial effects

Ghosh

Wang

et al. 2018

Tissue Barriers

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Curcumin has anti-inflammatory, anti-oxidant and anti-proliferative properties established largely by in vitro studies. Accordingly, oral administration of curcumin beneficially modulates many diseases including diabetes, fatty-liver disease, atherosclerosis, arthritis, cancer and neurological disorders such as depression, Alzheimer's or Parkinson's disease. However, limited bioavailability and inability to detect curcumin in circulation or target tissues has hindered the validation of a causal role. We established curcumin-mediated decrease in the release of gut bacteria-derived lipopolysaccharide (LPS) into circulation by maintaining the integrity of the intestinal barrier function as the mechanism underlying the attenuation of metabolic diseases (diabetes, atherosclerosis, kidney disease) by curcumin supplementation precluding the need for curcumin absorption. In view of the causative role of circulating LPS and resulting chronic inflammation in the development of diseases listed above, this review summarizes the mechanism by which curcumin affects the several layers of the intestinal barrier and, despite negligible absorption, can beneficially modulate these diseases.

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Vitamin D3 induces vitamin D receptor and HDAC11 binding to relieve the promoter of the tight junction proteins

Cited by 26 publications

References 28 publications

Vitamin D Receptor Deletion Leads to the Destruction of Tight and Adherens Junctions in Lungs

Vitamin D Receptor Deletion Leads to the Destruction of Tight and Adherens Junctions in Lungs

Vitamin D Modulates Intestinal Microbiota in Inflammatory Bowel Diseases

Curcumin-mediated regulation of intestinal barrier function: The mechanism underlying its beneficial effects

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