Evidence map›Paper›PMID 25502009›Full record

ArticleScientific reports2014

p38α (MAPK14) critically regulates the immunological response and the production of specific cytokines and chemokines in astrocytes.

U Lo, V Selvaraj, J M Plane, O V Chechneva, K Otsu, W Deng

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. 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
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

41 citing papers in PubMed, 65 citations in OpenAlex.

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  17. A compendium of validated pain genes.WIREs mechanisms of disease · 2022
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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

6 authors at 3 institutions in 3 countries.

U LoDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
V SelvarajDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
J M PlaneDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
O V ChechnevaDepartment of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA.
K OtsuDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, Japan.
W Deng1] Department of Biochemistry and Molecular Medicine, University of California, Davis, CA, USA [2] Medical College, Hubei University of Arts and Science, Xiangyang, Hubei, China [3] Shriners Institute for Pediatric Regenerative Medicine, Sacramento, CA, USA.
University of California, Davis · USHubei University of Arts and Science · CNOsaka University · JP

Funding

Oligodendrocytes, Glutamate Receptors, and Lead NeurotoxicityR01ES015988 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DENG, WENBIN · 2007 to 2011
$2.0M
NIEHS NIH HHS R01 ES015988NIEHS NIH HHS R01ES015988NINDS NIH HHS R01NS061983
6 · The paper itself

Abstract

In CNS lesions, "reactive astrocytes" form a prominent cellular response. However, the nature of this astrocyte immune activity is not well understood. In order to study astrocytic immune responses to inflammation and injury, we generated mice with conditional deletion of p38α (MAPK14) in GFAP+ astrocytes. We studied the role of p38α signaling in astrocyte immune activation both in vitro and in vivo, and simultaneously examined the effects of astrocyte activation in CNS inflammation. Our results showed that specific subsets of cytokines (TNFα, IL-6) and chemokines (CCL2, CCL4, CXCL1, CXCL2, CXCL10) are critically regulated by p38α signaling in astrocytes. In an in vivo CNS inflammation model of intracerebral injection of LPS, we observed markedly attenuated astrogliosis in conditional GFAPcre p38α(-/-) mice. However, GFAPcre p38α(-/-) mice showed marked upregulation of CCL2, CCL3, CCL4, CXCL2, CXCL10, TNFα, and IL-1β compared to p38αfl/fl cohorts, suggesting that in vivo responses to LPS after GFAPcre p38α deletion are complex and involve interactions between multiple cell types. This finding was supported by a prominent increase in macrophage/microglia and neutrophil recruitment in GFAPcre p38α(-/-) mice compared to p38αfl/fl controls. Together, these studies provide important insights into the critical role of p38α signaling in astrocyte immune activation.

Indexed as

AnimalsAstrocytesBrainCell Adhesion MoleculesCells, CulturedChemokinesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMAP-Kinase-Activated Kinase 2MAP Kinase Signaling SystemMice, KnockoutMitogen-Activated Protein Kinase 14NF-kappa BProtein Serine-Threonine KinasesCell Adhesion MoleculesChemokinesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLipopolysaccharidesMAP-Kinase-Activated Kinase 2Mitogen-Activated Protein Kinase 14NF-kappa BProtein Serine-Threonine Kinases

Identifiers

PMID25502009
PMCPMC4264013
OpenAlexW2001904531

What OpenQuestion holds

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LicenceCC BY
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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.