Evidence map›Paper›PMID 24393524›Full record

ArticleBMB reports2014

Role of NADH: quinone oxidoreductase-1 in the tight junctions of colonic epithelial cells.

Seung Taek Nam, Jung Hwan Hwang, Dae Hong Kim, Mi Jung Park, Ik Hwan Lee, Hyo Jung Nam, Jin Ku Kang, Sung Kuk Kim, Jae Sam Hwang, Hyo Kyun Chung and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. NADAntioxidants (Basel, Switzerland) · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019
    Article
  10. Article
  11. 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

13 authors at 2 institutions in 1 country.

Seung Taek NamDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Jung Hwan HwangLaboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 305-806, Korea.
Dae Hong KimDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Mi Jung ParkDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Ik Hwan LeeDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Hyo Jung NamDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Jin Ku KangDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Sung Kuk KimDepartment of Life Science, College of Natural Science, Daejin University, Pocheon 487-711, Korea.
Jae Sam HwangDepartment of Agricultural Biology, National Academy of Agricultural Science, RDA, Suwon 441-707, Korea.
Hyo Kyun ChungDepartment of Internal Medicine, Chungnam National University, Daejon 301-721, Korea.
Minho ShongDepartment of Internal Medicine, Chungnam National University, Daejon 301-721, Korea.
Chul-Ho LeeLaboratory Animal Resource Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 305-806, Korea.
Ho KimDepartment of Internal Medicine, Chungnam National University, Daejon 301-721, Korea.
Daejin University · KRNational Academy of Agricultural Science · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

nadhquinone oxidoreductase 1 (NQO1) is known to be involved in the regulation of energy synthesis and metabolism, and the functional studies of NQO1 have largely focused on metabolic disorders. Here, we show for the first time that compared to NQO1-WT mice, NQO1-KO mice exhibited a marked increase of permeability and spontaneous inflammation in the gut. In the DSS-induced colitis model, NQO1-KO mice showed more severe inflammatory responses than NQO1-WT mice. Interestingly, the transcript levels of claudin and occludin, the major tight junction molecules of gut epithelial cells, were significantly decreased in NQO1-KO mice. The colons of NQO1-KO mice also showed high levels of reactive oxygen species (ROS) and histone deacetylase (HDAC) activity, which are known to affect transcriptional regulation. Taken together, these novel findings indicate that NQO1 contributes to the barrier function of gut epithelial cells by regulating the transcription of tight junction molecules.

Indexed as

AnimalsCell Membrane PermeabilityCells, CulturedClaudin-1ColitisDisease Models, AnimalDown-RegulationEpithelial CellsHistone DeacetylasesMiceMice, KnockoutNAD(P)H Dehydrogenase (Quinone)OccludinReactive Oxygen SpeciesTight JunctionsClaudin-1Histone DeacetylasesNAD(P)H Dehydrogenase (Quinone)OccludinReactive Oxygen Species

Identifiers

PMID24393524
PMCPMC4206724
OpenAlexW2068995760

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.