Evidence map›Paper›PMID 20595622›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010

c-Jun NH2-terminal kinase-2 mediates osmotic stress-induced tight junction disruption in the intestinal epithelium.

G Samak, T Suzuki, A Bhargava, R K Rao

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. c-Jun N-Terminal Kinase-2 Mediates Alcohol and Corticosterone-Induced Tissue Injury at the Gut-Liver Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Cells · 2021
    Article
  10. The Epithelial Cell Leak Pathway.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

4 authors at 2 institutions in 1 country.

G SamakDepartment of Physiology, University of Tennessee Health Science Center, Memphis, 38163, USA.
T Suzuki
A Bhargava
R K Rao
University of Tennessee Health Science Center · USUniversity of California, San Francisco · US

Funding

INTESTINAL MUCOSAL PROTECTION BY EPIDERMAL GROWTH FACTORR01DK055532 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, RADHAKRISHNA · 1998 to 2020
$4.7M
Regulation and Function of Urocortins and their ReceptorsR01DK080787 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BHARGAVA, ADITI · 2009 to 2013
$2.2M
NIDDK NIH HHS R01 DK055532NIDDK NIH HHS R01 DK080787
6 · The paper itself

Abstract

Gastrointestinal epithelium faces osmotic stress, both at physiological and pathophysiological conditions. JNK activation is an immediate cellular response to osmotic stress. We investigated the effect of osmotic stress on intestinal epithelial barrier function and delineated the role of JNK2 in osmotic stress-induced tight junction (TJ) regulation in Caco-2 cell monolayers and ileum of Jnk(-/-) and Jnk2(-/-) mice. The role of JNK activation in osmotic stress-induced TJ disruption was evaluated using JNK-specific inhibitor and antisense oligonucleotides. Furthermore, the effect of cold restraint stress in vivo on TJ integrity was determined in rats. Osmotic stress disrupted TJs and barrier function in Caco-2 cell monolayers without affecting cell viability. Osmotic stress activated JNK1 and JNK2 and the inhibition of JNK by SP600125 attenuated osmotic stress-induced TJ disruption. TJ disruption and barrier dysfunction by osmotic stress was associated with JNK-dependent remodeling of actin cytoskeleton. Knockdown of JNK2 accelerated TJ assembly and attenuated osmotic stress-induced TJ disruption in Caco-2 cell monolayers. In mouse ileum in vitro, osmotic stress increased paracellular permeability, which was attenuated by SP600125. Osmotic stress disrupted actin cytoskeleton and TJs and increased paracellular permeability in the ileum of wild-type and JNK1(-/-) mice, but not in JNK2(-/-) mouse ileum. Cold restraint stress activated JNK in rat ileum and caused JNK-dependent remodeling of actin cytoskeleton and redistribution of occludin and zona occluden-1 from the intercellular junctions. These results reveal the role of JNK2 in the mechanism of osmotic stress-induced TJ disruption in the intestinal epithelium.

Indexed as

AnimalsCaco-2 CellsCalciumEpithelial CellsHumansIntestinal MucosaMaleMiceMice, KnockoutMitogen-Activated Protein Kinase 9Osmotic PressureProtein TransportRatsRats, Sprague-DawleyStress, PhysiologicalTight JunctionsCalciumMitogen-Activated Protein Kinase 9

Identifiers

PMID20595622
PMCPMC3774214
OpenAlexW2028691443

What OpenQuestion holds

Textmetadata
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.