Evidence map›Paper›PMID 26065916›Full record

ArticleScientific reports2015

Vitamin D3 inhibits lipopolysaccharide-induced placental inflammation through reinforcing interaction between vitamin D receptor and nuclear factor kappa B p65 subunit.

Yuan-Hua Chen, Zhen Yu, Lin Fu, Hua Wang, Xue Chen, Cheng Zhang, Zheng-Mei Lv, De-Xiang Xu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
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

39 citing papers in PubMed, 85 citations in OpenAlex.

  1. The Role of Vitamin D and Vitamin D Receptor in Sepsis.Current issues in molecular biology · 2025
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  10. Intramammary 25-hydroxyvitamin DJDS communications · 2023
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  12. Journal of pharmaceutical analysis · 2022
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  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 1 institution in 1 country.

Yuan-Hua Chen1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical University, Hefei, China [3] School of Basic Medical Science, Anhui Medical University, Hefei, 230032, China.
Zhen Yu1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical University, Hefei, China.
Lin FuSchool of Public Health, Anhui Medical University, Hefei, China.
Hua Wang1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical University, Hefei, China.
Xue ChenSchool of Public Health, Anhui Medical University, Hefei, China.
Cheng Zhang1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical University, Hefei, China.
Zheng-Mei LvSchool of Basic Medical Science, Anhui Medical University, Hefei, 230032, China.
De-Xiang Xu1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical University, Hefei, China.
Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is increasingly recognized that vitamin D3 (VitD3) has an anti-inflammatory activity. The present study investigated the effects of maternal VitD3 supplementation during pregnancy on LPS-induced placental inflammation and fetal intrauterine growth restriction (IUGR). All pregnant mice except controls were intraperitoneally injected with LPS (100 μg/kg) daily from gestational day (GD)15-17. In VitD3 + LPS group, pregnant mice were orally administered with VitD3 (25 μg/kg) before LPS injection. As expected, maternal LPS exposure caused placental inflammation and fetal IUGR. Interestingly, pretreatment with VitD3 repressed placental inflammation and protected against LPS-induced fetal IUGR. Further analysis showed that pretreatment with VitD3, which activated placental vitamin D receptor (VDR) signaling, specifically suppressed LPS-induced activation of nuclear factor kappa B (NF-κB) and significantly blocked nuclear translocation of NF-κB p65 subunit in trophoblast gaint cells of the labyrinth layer. Conversely, LPS, which activated placental NF-κB signaling, suppressed placental VDR activation and its target gene expression. Moreover, VitD3 reinforced physical interaction between placental VDR and NF-κB p65 subunit. The further study demonstrates that VitD3 inhibits placental NF-κB signaling in VDR-dependent manner. These results provide a mechanistic explanation for VitD3-mediated anti-inflammatory activity. Overall, the present study provides evidence for roles of VDR as a key regulator of placental inflammation.

Indexed as

Fetal Growth RetardationPlacentaPlacenta DiseasesAnimalsCholecalciferolFemaleInflammationLipopolysaccharidesMaleMiceMice, Inbred ICRPregnancyReceptors, CalcitriolSignal TransductionTranscription Factor RelACholecalciferolLipopolysaccharidesReceptors, CalcitriolRela protein, mouseTranscription Factor RelA

Identifiers

PMID26065916
PMCPMC4464284
OpenAlexW617789628

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.