Evidence map›Paper›PMID 33783968›Full record

ArticleActa physiologica (Oxford, England)2021

Chromogranin A regulates gut permeability via the antagonistic actions of its proteolytic peptides.

Elke M Muntjewerff, Kechun Tang, Lisanne Lutter, Gustaf Christoffersson, Mara J T Nicolasen, Hong Gao, Gajanan D Katkar, Soumita Das, Martin Ter Beest, Wei Ying and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Acta physiologica (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.4field-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

23 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Article
  3. The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Pathophysiology of Inflammatory Bowel Disease: Innate Immune System.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Observational
  20. Review
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

15 authors at 6 institutions in 3 countries.

Elke M MuntjewerffDepartment of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Kechun TangVA San Diego Healthcare System, San Diego, CA, USA.
Lisanne LutterCenter for Translational Immunology, Utrecht University Medical Center, Utrecht, the Netherlands.
Gustaf ChristofferssonScience for Life Laboratory, Uppsala University, Uppsala, Sweden.
Mara J T NicolasenDepartment of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Hong GaoDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Gajanan D KatkarDepartment of Cellular and Molecular Medicine, University of California San Diego, La Jolla, CA, USA.
Soumita DasDepartment of Pathology, University of California San Diego, La Jolla, CA, USA.
Martin Ter BeestDepartment of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Wei YingDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Pradipta GhoshDepartment of Medicine, University of California San Diego, La Jolla, CA, USA.
Sahar El AidyDepartment of Molecular Immunology and Microbiology, Groningen Biomolecular Sciences and Biotechnology Institute, University of Groningen, Groningen, the Netherlands.
Bas OldenburgDepartment of Gastroenterology and Hepatology, Utrecht University Medical Center, Utrecht, the Netherlands.
Geert van den BogaartDepartment of Tumor Immunology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, the Netherlands.
Sushil K MahataVA San Diego Healthcare System, San Diego, CA, USA.ORCID 0000-0002-8300-9873
University of California San Diego · USRadboud University Nijmegen · NLUtrecht University · NLUniversity of Groningen · NLUppsala University · SEVA San Diego Healthcare System · US

Funding

Modulation of Macrophage Polarization by Heterotrimeric G proteins: Implications of Gastrointestinal InflammationR01AI141630 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Pradipta Ghosh · 2019 to 2026
$3.2M
Catestatin improves glucose homeostasis and insulin sensitivity in diet-induced obese miceI01BX003934 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI MAHATA, SUSHIL K · 2018 to 2021
–
BLRD VA I01 BX003934NIAID NIH HHS R01 AI141630
6 · The paper itself

Abstract

aimA "leaky" gut barrier has been implicated in the initiation and progression of a multitude of diseases, for example, inflammatory bowel disease (IBD), irritable bowel syndrome and celiac disease. Here we show how pro-hormone Chromogranin A (CgA), produced by the enteroendocrine cells, and Catestatin (CST: hCgA

methodsColon tissues from region-specific CST-knockout (CST-KO) mice, CgA-knockout (CgA-KO) and WT mice were analysed by immunohistochemistry, western blot, ultrastructural and flowcytometry studies. FITC-dextran assays were used to measure intestinal barrier function. Mice were supplemented with CST or CgA fragment pancreastatin (PST: CgA

resultsPlasma levels of CST were elevated in IBD patients. CST-KO mice displayed (a) elongated tight, adherens junctions and desmosomes similar to IBD patients, (b) elevated expression of Claudin 2, and (c) gut inflammation. Plasma FITC-dextran measurements showed increased intestinal paracellular permeability in the CST-KO mice. This correlated with a higher ratio of Firmicutes to Bacteroidetes, a dysbiotic pattern commonly encountered in various diseases. Supplementation of CST-KO mice with recombinant CST restored paracellular permeability and reversed inflammation, whereas CgA-KO mice supplementation with CST and/or PST in CgA-KO mice showed that intestinal paracellular permeability is regulated by the antagonistic roles of these two peptides: CST reduces and PST increases permeability.

conclusionThe pro-hormone CgA regulates the intestinal paracellular permeability. CST is both necessary and sufficient to reduce permeability and primarily acts by antagonizing PST.

Indexed as

ColitisInflammatory Bowel DiseasesAnimalsChromogranin AHumansIntestinal MucosaMicePermeabilityTight JunctionsChromogranin ACatestatinchromogranin Aenteroendocrine cellsepithelial tight junctionsgut barrierinflammatory bowel disease

Identifiers

PMID33783968
PMCPMC8341099
OpenAlexW3140450030

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.