Evidence map›Paper›PMID 30345544›Full record

ArticleJournal of neuroscience research2019

AP-1 and the injury response of the GFAP gene.

Michael Brenner, Albee Messing, Michelle L Olsen

Abstract read
In one paragraph

Article in Journal of neuroscience research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Article
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  8. Article
  9. Article
  10. Article
  11. Review
  12. The Astrogenic Balance in the Aging Brain.Current neuropharmacology · 2021
    Review
  13. Article
  14. GFAP at 50.ASN neuro
    Review
  15. Review
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

3 authors at 3 institutions in 1 country.

Michael BrennerDepartment of Neurobiology and the Civitan International Research Center, Center for Glial Biology in Medicine, Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, Alabama.
Albee MessingDepartment of Comparative Biosciences, Waisman Center, University of Wisconsin-Madison, Madison, Wisconsin.
Michelle L OlsenSchool of Neuroscience, Virginia Polytechnic and State University, Blacksburg, Virginia.
Civitan International · USUniversity of Wisconsin–Madison · USVirginia Tech · US

Funding

ANALYSES AND APPLICATIONS OF GLIAL FIBRILLARY ACIDIC PROR01NS039055 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BRENNER, MICHAEL · 1999 to 2010
$2.6M
Epigenetic Regulation of Kir4.1 and GLT1 in PathophysiologyR01NS075062 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI OLSEN, MICHELLE L · 2013 to 2017
$1.6M
NINDS NIH HHS R01 NS039055NINDS NIH HHS R01 NS075062
6 · The paper itself

Abstract

Increased GFAP gene expression is a common feature of CNS injury, resulting in its use as a reporter to investigate mechanisms producing gliosis. AP-1 transcription factors are among those proposed to participate in mediating the reactive response. Prior studies found a consensus AP-1 binding site in the GFAP promoter to be essential for activity of reporter constructs transfected into cultured cells, but to have little to no effect on basal transgene expression in mice. Since cultured astrocytes display some properties of reactive astrocytes, these findings suggested that AP-1 transcription factors are critical for the upregulation of GFAP in injury, but not for its resting level of expression. We have examined this possibility by comparing the injury response in mice of lacZ transgenes driven by human GFAP promoters that contain the wild-type AP-1 binding site to those in which the site is mutated. An intact AP-1 site was found critical for a GFAP promoter response to the three different injury models used: physical trauma produced by cryoinjury, seizures produced by kainic acid, and chronic gliosis produced in an Alexander disease model. An unexpected additional finding was that the responses of the lacZ transgenes driven by the wild-type promoters were substantially less than that of the endogenous mouse GFAP gene. This suggests that the GFAP gene has previously unrecognized injury-responsive elements that reside further upstream of the transcription start site than the 2.2 kb present in the GFAP promoter segments used here.

Indexed as

AnimalsAstrocytesCells, CulturedGlial Fibrillary Acidic ProteinGliosisHumansMiceMice, Inbred C57BLMice, TransgenicPromoter Regions, GeneticTranscription Factor AP-1Glial Fibrillary Acidic ProteinTranscription Factor AP-1agingAlexander diseasebrain injuriescold injuryfemalegeneticglial fibrillary acidic proteingliosiskainic acidmiceRRID:IMSR_JAX:003487RRID:IMSR_TAC:fvbseizuressex characteristicsSTAT3 transcription factortranscriptiontranscription factor AP-1transgenic

Identifiers

PMID30345544
PMCPMC6289842
OpenAlexW2896079960

What OpenQuestion holds

Textmetadata
LicenceTDM
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.