Evidence map›Paper›PMID 29483282›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

BMP-Responsive Protease HtrA1 Is Differentially Expressed in Astrocytes and Regulates Astrocytic Development and Injury Response.

Jessie Chen, Stephanie Van Gulden, Tammy L McGuire, Andrew C Fleming, Chio Oka, John A Kessler, Chian-Yu Peng

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. 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
2.7field-weighted citation impact, top 11% 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, 27 citations in OpenAlex.

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  17. Novel mutation inNeurology. Genetics · 2019
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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

7 authors at 2 institutions in 2 countries.

Jessie ChenDepartment of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, Illinois 60611.ORCID 0000-0001-6943-6046
Stephanie Van GuldenDepartment of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, Illinois 60611.
Tammy L McGuireDepartment of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, Illinois 60611.
Andrew C FlemingDepartment of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, Illinois 60611.
Chio OkaGraduate School of Biological Sciences, Nara Institute of Science and Technology, Ikoma, Nara 630-192, Japan.ORCID 0000-0001-9352-461X
John A KesslerDepartment of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, Illinois 60611.ORCID 0000-0003-1948-7712
Chian-Yu PengDepartment of Neurology, Northwestern University's Feinberg School of Medicine, Chicago, Illinois 60611, c-peng@northwestern.edu.ORCID 0000-0003-3407-0894
Northwestern University · USNara Institute of Science and Technology · JP

Funding

Mentoring For Success: Developing Fundamental Skills For Biomedical ResearchR25GM079300 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MCGEE, RICHARD · 2007 to 2020
$6.6M
REGULATION OF NEUROTRANSMITTER METABOLISMR01NS020778 · NINDS · YESHIVA UNIVERSITY · PI KESSLER, JOHN A · 1985 to 2014
$4.6M
TRAINING PROGRAM IN ONCOGENESIS &DEVELOPMENT BIOLOGYT32CA080621 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI EKLUND, ELIZABETH ANN · 2001 to 2018
$4.1M
NCI NIH HHS T32 CA080621NIGMS NIH HHS R25 GM079300NINDS NIH HHS R01 NS020778
6 · The paper itself

Abstract

Astrocytes perform a wide array of physiological functions, including structural support, ion exchange, and neurotransmitter uptake. Despite this diversity, molecular markers that label subpopulations of astrocytes are limited, and mechanisms that generate distinct astrocyte subtypes remain unclear. Here we identified serine protease high temperature requirement A 1 (HtrA1), a bone morphogenetic protein 4 signaling regulated protein, as a novel marker of forebrain astrocytes, but not of neural stem cells, in adult mice of both sexes. Genetic deletion of HtrA1 during gliogenesis accelerates astrocyte differentiation. In addition, ablation of HtrA1 in cultured astrocytes leads to altered chondroitin sulfate proteoglycan expression and inhibition of neurite extension, along with elevated levels of transforming growth factor-β family proteins. Brain injury induces HtrA1 expression in reactive astrocytes, and loss of HtrA1 leads to an impairment in wound closure accompanied by increased proliferation of endothelial and immune cells. Our findings demonstrate that HtrA1 is differentially expressed in adult mouse forebrain astrocytes, and that HtrA1 plays important roles in astrocytic development and injury response.

Indexed as

NeurogenesisWound HealingAnimalsAstrocytesCell ProliferationCells, CulturedChondroitin Sulfate ProteoglycansFemaleHigh-Temperature Requirement A Serine Peptidase 1MaleMiceMice, Inbred C57BLProsencephalonTransforming Growth Factor betaChondroitin Sulfate ProteoglycansHigh-Temperature Requirement A Serine Peptidase 1HtrA1 protein, mouseTransforming Growth Factor betaastrocyte heterogeneitybone morphogenetic proteinbrain injurycerebrovascular diseasegliogenesisHtrA1

Identifiers

PMID29483282
PMCPMC5896000
OpenAlexW2788920981

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.