Evidence map›Paper›PMID 22466098›Full record

ArticleDigestive diseases and sciences2012

Inhibition of Pim-1 kinase ameliorates dextran sodium sulfate-induced colitis in mice.

Yue-Ming Shen, Yan Zhao, Ya Zeng, Lu Yan, Bo-Lin Chen, Ai-Min Leng, Yi-Bin Mu, Gui-Ying Zhang

Abstract read
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Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. The role of Pim-1 kinases in inflammatory signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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  12. The Role of NLRP3 Inflammasome in Lupus Nephritis.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Article
  15. The role of Pim kinase in immunomodulation.American journal of cancer research · 2020
    Review
  16. Article
  17. Article
  18. 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

8 authors at 4 institutions in 1 country.

Yue-Ming ShenDepartment of Gastroenterology, Xiangya Hospital, Central South University, Changsha, People's Republic of China.
Yan Zhao
Ya Zeng
Lu Yan
Bo-Lin Chen
Ai-Min Leng
Yi-Bin Mu
Gui-Ying Zhang
Central South University · CNXiangya Hospital Central South University · CNChangsha Central Hospital · CNFourth Hospital of Changsha · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPim-1 kinase is involved in the control of cell growth, differentiation and apoptosis. Recent evidence suggests that Pim kinases play a role in immune regulation and inflammation. However, the role of Pim-1 kinase in inflammatory bowel diseases (IBD) remains unclear.

aimsThe aims of this study were to explore the role of Pim-1 kinase in the pathology of IBD and to assess whether inhibiting Pim-1 kinase may be of therapeutic benefit as a treatment regimen for IBD.

methodsColitic mouse model was established by the induction of dextran sodium sulfate. The expression of Pim-1 in the colonic samples of control and colitic mice was examined. Furthermore, the mice were treated with Pim-1inhibitor (PIM-Inh), then the body weight and colon inflammation were evaluated, and the production of cytokines including IFN-γ, IL-4, TGF-β and IL-17 in colon tissues was determined by ELISA. The expression of T cell master transcription factors T-bet, ROR-γt, GATA-3 and Foxp3 and Nuclear factor κB (NF-κB) and inducible nitric oxide synthase in colon tissues was detected by real-time PCR and western blot. Finally, the effect of LPS on Pim-1 expression and the effects of PIM-Inh on LPS-induced upregualtion of p65 and TNF-α in RAW264.7 cells were examined by real-time PCR and western blot.

resultsPim-1 expression was correlated with the degree of mucosal inflammation in vivo, and it was significantly induced by LPS in vitro. PIM-Inh had protective effects on acute colitis in vivo. Mechanistically, PIM-Inh reduced the proinflammatory immune response through the inhibition of the overactivation of macrophages and the down-regulation of excessive Th1- and Th17-type immune responses. Furthermore, PIM-Inh could skew T cell differentiation towards a Treg phenotype.

conclusionsPim-1 kinase is involved in mucosal injury/inflammation and Pim-1 kinase inhibitor may provide a novel therapeutic approach for IBD.

Indexed as

AnimalsCells, CulturedColitisColonCytokinesDextran SulfateDisease Models, AnimaleIF-2 KinaseEnzyme InhibitorsIn Vitro TechniquesLipopolysaccharidesMacrophagesMaleMiceMice, Inbred BALB CProto-Oncogene Proteins c-pim-1CytokinesDextran SulfateeIF-2 KinaseEnzyme InhibitorsLipopolysaccharidesProto-Oncogene Proteins c-pim-1Transcription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID22466098
OpenAlexW2038704818

What OpenQuestion holds

Textmetadata
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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.