Evidence map›Paper›PMID 19220323›Full record

ArticleClinical and experimental immunology2009

The effect of proteasome inhibitor MG132 on experimental inflammatory bowel disease.

S Inoue, H Nakase, M Matsuura, S Mikami, S Ueno, N Uza, T Chiba

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 60 citations in OpenAlex.

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  14. IL-13 Impairs Tight Junctions in Airway Epithelia.International journal of molecular sciences · 2019
    Article
  15. Article
  16. Inhibition of ubiquitin-activating enzyme protects against organ injury after intestinal ischemia-reperfusion.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  17. Article
  18. Article
  19. Cancer cachexia-when proteasomal inhibition is not enough.Journal of cachexia, sarcopenia and muscle · 2016
    Article
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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

7 authors at 1 institution in 1 country.

S InoueDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
H Nakase
M Matsuura
S Mikami
S Ueno
N Uza
T Chiba
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoproteasome up-regulation enhances the processing of nuclear factor-kappaB (NF-kappaB) and degradation of IkappaBalpha, which correlates with increased amounts of NF-kappaB in the various cells. Aberrant activation of NF-kappaB is involved in the pathogenesis of inflammatory bowel disease (IBD). The aim of this study was to elucidate the effect of proteasome inhibitor MG132 on experimental IBD. We investigated the effects of MG132 on intestinal inflammation and epithelial regeneration in both interleukin-10-deficient (IL-10(-/-)) mice and mice with dextran sulphate sodium (DSS)-induced colitis. Body weight, histological findings and tumour necrosis factor (TNF)-alpha mRNA expression, epithelial cell proliferation and NF-kappaB p65 activity in colonic tissues were examined. The effects of MG132 on cell proliferation, migration and multiple drug resistance 1 (MDR1) gene expression were determined in vitro. MG132 ameliorated intestinal inflammation of IL-10(-/-) mice by decreasing TNF-alpha mRNA expression in the colonic tissues, which was associated with suppression of NF-kappaB activation, and reduced significantly the number of Ki-67-positive intestinal epithelial cells. On the other hand, MG132 did not reduce intestinal inflammation in mice with DSS-induced colitis, and delayed significantly the recovery of body weight and epithelial regeneration. MG132 also suppressed significantly epithelial cell proliferation, cell migration and MDR1 gene expression in vitro. Proteasome inhibition reduces T cell-mediated intestinal inflammation, but may interrupt both epithelial regeneration and barrier function of colonic mucosa. Optimal use of proteasome inhibitor should be kept in mind when we consider its clinical application for patients with IBD.

Indexed as

AnimalsCell ProliferationColonCysteine Proteinase InhibitorsDextran SulfateDisease Models, AnimalDose-Response Relationship, DrugDrug Evaluation, PreclinicalFemaleGene Expression RegulationInflammatory Bowel DiseasesInterleukin-10Intestinal MucosaLeupeptinsMiceMice, Inbred C57BLbenzyloxycarbonylleucyl-leucyl-leucine aldehydeCysteine Proteinase InhibitorsDextran SulfateInterleukin-10LeupeptinsRNA, MessengerTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID19220323
PMCPMC2673755
OpenAlexW1981985646

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.