Evidence map›Paper›PMID 24252623›Full record

ArticleActa neuropathologica communications2013

Astrocytes differentially respond to inflammatory autoimmune insults and imbalances of neural activity.

Peter Jukkola, Tomas Guerrero, Victoria Gray, Chen Gu

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  11. Treatment with an antigen-specific dual microparticle system reverses advanced multiple sclerosis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022
    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

4 authors at 1 institution in 1 country.

Peter JukkolaBiomedical Sciences Graduate Program, The Ohio State University, Columbus, OH 43210, USA. gu.49@osu.edu.
Tomas Guerrero
Victoria Gray
Chen Gu
The Ohio State University · US

Funding

Mechanism and function of Kv channel targetingR01NS062720 · NINDS · OHIO STATE UNIVERSITY · PI GU, CHEN · 2009 to 2013
$1.4M
NINDS NIH HHS R01 NS062720
6 · The paper itself

Abstract

backgroundNeuronal activity intimately communicates with blood flow through the blood-brain barrier (BBB) in the central nervous system (CNS). Astrocyte endfeet cover more than 90% of brain capillaries and interact with synapses and nodes of Ranvier. The roles of astrocytes in neurovascular coupling in the CNS remain poorly understood.

resultsHere we show that astrocytes that are intrinsically different are activated by inflammatory autoimmune insults and alterations of neuronal activity. In the progression of experimental autoimmune encephalomyelitis (EAE), both fibrous and protoplasmic astrocytes were broadly and reversibly activated in the brain and spinal cord, indicated by marked upregulation of glial fibrillary acidic protein (GFAP) and other astrocytic proteins. In early and remitting EAE, upregulated GFAP and astrocytic endfoot water channel aquaporin 4 (AQP4) enclosed white matter lesions in spinal cord, whereas they markedly increased and formed bundles in exacerbated lesions in late EAE. In cerebellar cortex, upregulation of astrocytic proteins correlated with EAE severity. On the other hand, protoplasmic astrocytes were also markedly activated in the brains of ankyrin-G (AnkG) and Kv3.1 KO mice, where neuronal activities are altered. Massive astrocytes replaced degenerated Purkinje neurons in AnkG KO mice. In Kv3.1 KO mice, GFAP staining significantly increased in cerebellar cortex, where Kv3.1 is normally highly expressed, but displayed in a patchy pattern in parts of the hippocampus.

conclusionsThus, astrocytes can detect changes in both blood and neurons, which supports their central role in neurovascular coupling. These studies contribute to the development of new strategies of neuroprotection and repair for various diseases, through activity-dependent regulation of neurovascular coupling.

Indexed as

AnimalsAnkyrinsAquaporin 4AstrocytesBacterial ProteinsBrainChronic DiseaseEncephalomyelitis, Autoimmune, ExperimentalFemaleGlial Fibrillary Acidic ProteinLuminescent ProteinsMice, Inbred C57BLMice, KnockoutMice, TransgenicMyelin SheathNeuronsAnk3 protein, mouseAnkyrinsAqp4 protein, mouseAquaporin 4Bacterial ProteinsGlial Fibrillary Acidic ProteinKcnc1 protein, mouseLuminescent ProteinsShaw Potassium ChannelsVimentinyellow fluorescent protein, Bacteria

Identifiers

PMID24252623
PMCPMC3893391
OpenAlexW2061330716

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.