Evidence map›Paper›PMID 33273633›Full record

ArticleScientific reports2020

Mucin-2 knockout is a model of intercellular junction defects, mitochondrial damage and ATP depletion in the intestinal epithelium.

Mariya A Borisova, Kseniya M Achasova, Ksenia N Morozova, Evgeniya N Andreyeva, Ekaterina A Litvinova, Anna A Ogienko, Maryana V Morozova, Mariya B Berkaeva, Elena Kiseleva, Elena N Kozhevnikova

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
9.5field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 82 citations in OpenAlex.

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  12. Metabolites · 2025
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  18. Underneath the Gut-Brain Axis in IBD-Evidence of the Non-Obvious.International journal of molecular sciences · 2024
    Review
  19. Article
  20. Acta pharmaceutica Sinica. B · 2024
    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 at 3 institutions in 1 country.

Mariya A BorisovaThe Federal Research Center Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Kseniya M AchasovaInstitute of Molecular and Cellular Biology, The Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Ksenia N MorozovaThe Federal Research Center Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Evgeniya N AndreyevaInstitute of Molecular and Cellular Biology, The Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Ekaterina A LitvinovaScientific Research Institute of Physiology and Basic Medicine, Novosibirsk, Russian Federation, 630117.
Anna A OgienkoInstitute of Molecular and Cellular Biology, The Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Maryana V MorozovaInstitute of Molecular and Cellular Biology, The Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Mariya B BerkaevaInstitute of Molecular and Cellular Biology, The Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Elena KiselevaThe Federal Research Center Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090.
Elena N KozhevnikovaInstitute of Molecular and Cellular Biology, The Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russian Federation, 630090. kozhevnikovaen@physiol.ru.
Siberian Branch of the Russian Academy of Sciences · RUInstitute of Cytology and Genetics · RUInstitute of Physiology and Basic Medicine · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The disruption of the protective intestinal barrier-the 'leaky gut'-is a common complication of the inflammatory bowel disease. There is limited data on the mechanisms of the intestinal barrier disruption upon low-grade inflammation characteristic of patients with inflammatory bowel disease in clinical remission. Thus, animal models that recapitulate the complexity of chronic intestinal inflammation in vivo are of particular interest. In this study, we used Mucin-2 (Muc2) knockout mice predisposed to colitis to study intestinal barrier upon chronic inflammation. We used 4-kDa FITC-Dextran assay and transmission electron microscopy to demonstrate the increased intestinal permeability and morphological defects in intercellular junctions in Muc2 knockout mice. Confocal microscopy revealed the disruption of the apical F-actin cytoskeleton and delocalization of tight junction protein Claudin-3 from the membrane. We further demonstrate mitochondrial damage, impaired oxygen consumption and the reduction of the intestinal ATP content in Muc2 knockout mice. Finally, we show that chemically induced mitochondrial uncoupling in the wild type mice mimics the intestinal barrier disruption in vivo and causes partial loss of F-actin and membrane localization of Claudin-3. We propose that mitochondrial damage and metabolic shifts during chronic inflammation contribute to the leaky gut syndrome in Muc2 knockout animal model of colitis.

Indexed as

Adenosine TriphosphateAnimalsColitisDisease Models, AnimalHumansIntestinal MucosaMiceMice, KnockoutMitochondriaMucin-2Tight JunctionsAdenosine TriphosphateMUC2 protein, humanMucin-2

Identifiers

PMID33273633
PMCPMC7713437
OpenAlexW3108325352

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.