Evidence map›Paper›PMID 22637476›Full record

ArticleThe Journal of biological chemistry2012

Mechanism for p38α-mediated experimental autoimmune encephalomyelitis.

Kana Namiki, Hirofumi Matsunaga, Kento Yoshioka, Kensuke Tanaka, Kazuya Murata, Junji Ishida, Akira Sakairi, Jundal Kim, Naoki Tokuhara, Nobuhiko Shibakawa and 9 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Go-sha-jinki-Gan Alleviates Inflammation in Neurological Disorders via p38-TNF Signaling in the Central Nervous System.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  4. Article
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  6. Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    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

19 authors at 4 institutions in 1 country.

Kana NamikiDepartment of Biochemistry and Molecular Pharmacology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
Hirofumi Matsunaga
Kento Yoshioka
Kensuke Tanaka
Kazuya Murata
Junji Ishida
Akira Sakairi
Jundal Kim
Naoki Tokuhara
Nobuhiko Shibakawa
Motohisa Shimizu
Yukinori Wada
Yasunori Tokunaga
Manabu Shigetomi
Masahiko Hagihara
Sadao Kimura
Tatsuhiko Sudo
Akiyoshi Fukamizu
Yoshitoshi Kasuya
Ube (Japan) · JPChiba University · JPUniversity of Tsukuba · JPRIKEN Advanced Science Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the mitogen-activated protein kinases, p38, has been found to play a crucial role in various inflammatory responses. In this study, we analyzed the roles of p38α in multiple sclerosis, using an animal model, experimental autoimmune encephalomyelitis (EAE). p38α(+/-) mice (p38α(-/-) showed embryonic lethality) showed less severe neurological signs than WT mice. Adoptive transfer of lymph node cells (LNC) from sensitized WT mice with MOG(35-55) to naive WT-induced EAE was much more severe compared with the case using LNC from sensitized p38α(+/-) mice. Comprehensive analysis of cytokines from MOG(35-55)-challenged LNC by Western blot array revealed that production of IL-17 was significantly reduced by a single copy disruption of the p38α gene or a p38 inhibitor. Likewise, by a luciferase reporter assay, an electrophoresis mobility shift assay, and characterization of the relationship between p38 activity and IL-17 mRNA expression, we confirmed that p38 positively regulates transcription of the Il17 gene. Furthermore, oral administration of a highly specific p38α inhibitor (UR-5269) to WT mice at the onset of EAE markedly suppressed the progression of EAE compared with a vehicle group. These results suggest that p38α participates in the pathogenesis of EAE through IL-17 induction.

Indexed as

AnimalsElectrophoretic Mobility Shift AssayEncephalomyelitis, Autoimmune, ExperimentalEnzyme InhibitorsFemaleInterleukin-17MaleMiceMitogen-Activated Protein Kinase 14Promoter Regions, GeneticRNA StabilityEnzyme InhibitorsInterleukin-17Mitogen-Activated Protein Kinase 14

Identifiers

PMID22637476
PMCPMC3397849
OpenAlexW2084327854

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.