Evidence map›Paper›PMID 28938596›Full record

ArticleOncotarget2017

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

Feng-Hua Liu, Shan-Shan Li, Xiao-Xi Li, Shuai Wang, Mao-Gang Li, Li Guan, Tian-Gang Luan, Zhi-Gang Liu, Zhan-Ju Liu, Ping-Chang Yang

Abstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Vitamin DStem cell research & therapy · 2021
    Article
  12. Article
  13. Review
  14. Vitamin D Modulates Intestinal Microbiota in Inflammatory Bowel Diseases.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Feng-Hua LiuThe Department of Gastroenterology, The Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, China.
Shan-Shan LiThe Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.
Xiao-Xi LiThe Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.
Shuai WangThe Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.
Mao-Gang LiThe Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.
Li GuanAffiliated Luohu Hospital, Shenzhen University, Shenzhen 518001, China.
Tian-Gang LuanAffiliated Luohu Hospital, Shenzhen University, Shenzhen 518001, China.
Zhi-Gang LiuThe Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.
Zhan-Ju LiuThe Department of Gastroenterology, The Shanghai Tenth People's Hospital of Tongji University, Shanghai 200072, China.
Ping-Chang YangThe Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal epithelial barrier dysfunction and vitamin D (VitD)-deficiency play a critical role in a large number of diseases. The histone deacetylases (HDAC) are associated with a large number of immune diseases. This study tests a hypothesis that the interaction between VitD and HDAC is associated with the regulation of epithelial barrier functions. In this study, human intestinal epithelial cell line, T84 cells, was cultured into monolayers to be used as a model to test the epithelial barrier functions. We observed that in a VitD-deficient environment, the T84 monolayer barrier function was compromised. Exposure to calcitriol (the active form of VitD3) in the culture increased the expression of VitD receptor (VDR) in T84 cells. In a VitD-sufficient environment, VDR formed a complex with histone deacetylase-11 (HDAC11); the complex was markedly decreased in a VitD-deficient environment. We also observed that significantly more binding of HDAC11 to the promoter of the tight junction proteins inhibit the gene transcription activities of these loci in the VitD-deficient environment, which were abolished by the presence of calcitriol in the culture. In conclusion, the interaction between VDR and HDAC11 plays a crucial role in the maintenance of the epithelial barrier integrity.

Indexed as

barrier functionepitheliumhistone deacetylaseintestinevitamin D

Identifiers

PMID28938596
PMCPMC5601692

What OpenQuestion holds

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Registered trials

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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.