Evidence map›Paper›PMID 28484281›Full record

ArticleScientific reports2017

Intestinal Epithelial Cell-Specific Deletion of PLD2 Alleviates DSS-Induced Colitis by Regulating Occludin.

Chaithanya Chelakkot, Jaewang Ghim, Nirmal Rajasekaran, Jong-Sun Choi, Jung-Hwan Kim, Myoung Ho Jang, Young Kee Shin, Pann-Ghill Suh, Sung Ho Ryu

Abstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Ion transport and epithelial barrier dysfunction in experimental models of ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  3. Heat-killedJournal of clinical biochemistry and nutrition · 2025
    Article
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  14. Regulation, targets and functions of CSK.Frontiers in cell and developmental biology · 2023
    Review
  15. Article
  16. Article
  17. Review
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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

9 authors.

Chaithanya ChelakkotDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, San 31, Hyoja-Dong, Pohang, Gyeongsanbuk- do, 37673, South Korea.
Jaewang GhimDepartment of Life Science, Pohang University of Science and Technology, San 31, Hyoja-Dong, Pohang, Gyeongsanbuk- do, 37673, South Korea.
Nirmal RajasekaranLaboratory of Molecular Pathology and Cancer Genomics, College of Pharmacy, Seoul National University, Seoul, 08826, South Korea.
Jong-Sun ChoiThe Center for Anti-cancer Companion Diagnostics, Institutes of Entrepreneurial Bio-Convergence, Seoul National University, Seoul, 08826, South Korea.
Jung-Hwan KimDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, San 31, Hyoja-Dong, Pohang, Gyeongsanbuk- do, 37673, South Korea.
Myoung Ho JangDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, San 31, Hyoja-Dong, Pohang, Gyeongsanbuk- do, 37673, South Korea.
Young Kee ShinLaboratory of Molecular Pathology and Cancer Genomics, College of Pharmacy, Seoul National University, Seoul, 08826, South Korea.
Pann-Ghill SuhSchool of Life Science, Ulsan National Institute of Science and Technology, Ulsan, 44919, South Korea.
Sung Ho RyuDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, San 31, Hyoja-Dong, Pohang, Gyeongsanbuk- do, 37673, South Korea. sungho@postech.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ulcerative colitis is a multi-factorial disease involving a dysregulated immune response. Disruptions to the intestinal epithelial barrier and translocation of bacteria, resulting in inflammation, are common in colitis. The mechanisms underlying epithelial barrier dysfunction or regulation of tight junction proteins during disease progression of colitis have not been clearly elucidated. Increase in phospholipase D (PLD) activity is associated with disease severity in colitis animal models. However, the role of PLD2 in the maintenance of intestinal barrier integrity remains elusive. We have generated intestinal-specific Pld2 knockout mice (Pld2 IEC-KO) to investigate the mechanism of intestinal epithelial PLD2 in colitis. We show that the knockout of Pld2 confers protection against dextran sodium sulphate (DSS)-induced colitis in mice. Treatment with DSS induced the expression of PLD2 and downregulated occludin in colon epithelial cells. PLD2 was shown to mediate phosphorylation of occludin and induce its proteasomal degradation in a c-Src kinase-dependent pathway. Additionally, we have shown that treatment with an inhibitor of PLD2 can rescue mice from DSS-induced colitis. To our knowledge, this is the first report showing that PLD2 is pivotal in the regulation of the integrity of epithelial tight junctions and occludin turn over, thereby implicating it in the pathogenesis of colitis.

Indexed as

Gene DeletionAnimalsColitisDextran SulfateDinitrofluorobenzeneDown-RegulationEpithelial CellsHT29 CellsHumansIntestinesMice, Inbred C57BLMice, KnockoutModels, BiologicalOccludinOrgan SpecificityPhospholipase D2,4-dinitrofluorobenzene sulfonic acidDextran SulfateDinitrofluorobenzeneOccludinPhospholipase Dphospholipase D2Proteasome Endopeptidase Complexsrc-Family Kinases

Identifiers

PMID28484281
PMCPMC5431506

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.