Evidence map›Paper›PMID 29238610›Full record

ArticleCell discovery2017

A role for ErbB signaling in the induction of reactive astrogliosis.

Jing Chen, Wanwan He, Xu Hu, Yuwen Shen, Junyan Cao, Zhengdong Wei, Yifei Luan, Li He, Fangdun Jiang, Yanmei Tao

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.2field-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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 1 institution in 1 country.

Jing ChenInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Wanwan HeInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Xu HuInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Yuwen ShenInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Junyan CaoInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Zhengdong WeiInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Yifei LuanInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Li HeInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Fangdun JiangInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Yanmei TaoInstitute of Life Sciences, College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.ORCID 0000-0002-4456-5447
Hangzhou Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive astrogliosis is a hallmark of many neurological disorders, yet its functions and molecular mechanisms remain elusive. Particularly, the upstream signaling that regulates pathological responses of astrocytes is largely undetermined. We used a mouse traumatic brain injury model to induce astrogliosis and revealed activation of ErbB receptors in reactive astrocytes. Moreover, cell-autonomous inhibition of ErbB receptor activity in reactive astrocytes by a genetic approach suppressed hypertrophic remodeling possibly through the regulation of actin dynamics. However, inhibiting ErbB signaling in reactive astrocytes did not affect astrocyte proliferation after brain injury, although it aggravated local inflammation. In contrast, active ErbB signaling in mature astrocytes of various brain regions in mice was sufficient to initiate reactive responses, reproducing characterized molecular and cellular features of astrogliosis observed in injured or diseased brains. Further, prevalent astrogliosis in the brain induced by astrocytic ErbB activation caused anorexia in animals. Therefore, our findings defined an unrecognized role of ErbB signaling in inducing reactive astrogliosis. Mechanistically, inhibiting ErbB signaling in reactive astrocytes prominently reduced Src and focal adhesion kinase (FAK) activity that is important for actin remodeling, although ErbB signaling activated multiple downstream signaling proteins. The discrepancies between the results from loss- and gain-of-function studies indicated that ErbB signaling regulated hypertrophy and proliferation of reactive astrocytes by different downstream signaling pathways. Our work demonstrated an essential mechanism in the pathological regulation of astrocytes and provided novel insights into potential therapeutic targets for astrogliosis-implicated diseases.

Indexed as

anorexiabrain injurygliagliosisreceptor tyrosine kinase

Identifiers

PMID29238610
PMCPMC5717352
OpenAlexW2775238973

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.