Evidence map›Paper›PMID 29693124›Full record

ArticleMolecular medicine reports2018

Regulation of the expression of tumor necrosis factor‑related genes by abnormal histone H3K27 acetylation: Implications for neural tube defects.

Chunlei Wan, Xiaozhen Liu, Baoling Bai, Haiyan Cao, Huili Li, Qin Zhang

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 50% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Chunlei WanBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing 100020, P.R. China.
Xiaozhen LiuBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing 100020, P.R. China.
Baoling BaiBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing 100020, P.R. China.
Haiyan CaoBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing 100020, P.R. China.
Huili LiBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing 100020, P.R. China.
Qin ZhangBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Peking University Teaching Hospital, Beijing 100020, P.R. China.
Capital Institute of Pediatrics · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The association between apoptosis and neural tube defects (NTDs) is recognized as important, however, the precise link remains to be elucidated. Epigenetic modifications in human NTDs have been detected previously. In the present study, the occurrence of epigenetic modifications in apoptosis‑related genes was investigated in a retinoic acid (RA)‑induced mouse NTD model. Among 84 key genes involved in programmed cell death, 13 genes, including tumor necrosis factor (Tnf), annexin A5, apoptosis inhibitor 5, Bcl2‑associated athanogene 3, baculoviral IAP repeat‑containing 3, caspase (Casp)12, Casp4, Casp8, lymphotoxin β receptor, NLR family, apoptosis inhibitory protein 2, TNF receptor superfamily (Tnfrsf)1a, TNF superfamily (Tnfs)f10 and Tnfsf12, were downregulated, whereas nucleolar protein 3 was upregulated in the RA‑induced NTD mice. Chromatin immunoprecipitation assays revealed that the regulatory regions of these differentially expressed TNF‑related genes showed reduced histone H3K27 acetylation in NTDs, compared with control mice without NTDs. Reverse transcription‑quantitative polymerase chain reaction revealed that H3K27ac‑binding to the differentially regulated genes was markedly decreased in the NTD mice, whereas binding to the unchanged genes Casp3 and Nfkb1 was unaffected. In conclusion, certain TNF‑related genes appeared to be downregulated in NTDs, possibly as a result of abnormal histone H3K27 acetylation. These results shed new light on the epigenetic dysregulation of apoptosis‑related genes in NTDs.

Indexed as

Gene Expression Regulation, DevelopmentalAcetylationAnimalsApoptosisChromatin ImmunoprecipitationEpigenesis, GeneticFemaleGene Expression ProfilingGenomicsHistonesMaleMiceNeural Tube DefectsPromoter Regions, GeneticSignal TransductionTranscriptomeHistonesTumor Necrosis Factors

Identifiers

PMID29693124
PMCPMC5983976
OpenAlexW2800648584

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.