Evidence map›Paper›PMID 25736717›Full record

ArticleScientific reports2015

βA3/A1-crystallin is a critical mediator of STAT3 signaling in optic nerve astrocytes.

Mallika Valapala, Malia Edwards, Stacey Hose, Jianfei Hu, Eric Wawrousek, Gerard A Lutty, J Samuel Zigler, Jiang Qian, Debasish Sinha

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Involvement of Anoikis in Dissociated Optic Nerve Fiber Layer Appearance.International journal of molecular sciences · 2021
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
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

9 authors at 3 institutions in 1 country.

Mallika ValapalaWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Malia EdwardsWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Stacey HoseWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Jianfei HuWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Eric WawrousekNational Eye Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Gerard A LuttyWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
J Samuel ZiglerWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Jiang QianWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Debasish SinhaWilmer Eye Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA.
Johns Hopkins Medicine · USJohns Hopkins University · USNational Institutes of Health · US

Funding

NEI Genetic Engineering CoreZICEY000458 · NEI · NATIONAL EYE INSTITUTE · PI DONG, LIJIN · 2009 to 2025
$22.6M
Wilmer Core Grant for Vision ResearchP30EY001765 · NEI · JOHNS HOPKINS UNIVERSITY · PI Jiang Qian · 1985 to 2026
$22.1M
Vasculogenesis and hyperoxia in the developing retina.R01EY009357 · NEI · JOHNS HOPKINS UNIVERSITY · PI LUTTY, GERARD ANTHONY · 1993 to 2014
$5.3M
A novel bA3/A1-crystallin gene mutation results in persistent fetal vasculatureR01EY019037 · NEI · JOHNS HOPKINS UNIVERSITY · PI SINHA, DEBASISH · 2008 to 2015
$4.1M
NEI NIH HHS EY009357NEI NIH HHS EY019037NEI NIH HHS EY019037-SNEI NIH HHS P30 EY001765NEI NIH HHS R01 EY009357NEI NIH HHS R01 EY019037
6 · The paper itself

Abstract

We have previously reported that in the Nuc1 rat, which has a spontaneous mutation in Cryba1 (the gene encoding βA3/A1-crystallin), astrocytes exhibit decreased Notch signaling, leading to reduced promoter activity for glial fibrillary acidic protein (GFAP). Interestingly, in both Nuc1 astrocytes and in wild type astrocytes following knockdown of Cryba1, vascular endothelial growth factor (VEGF) secretion is decreased. This has led us to explore signaling mediators that could be regulated by βA3/A1-crystallin to modulate both GFAP and VEGF. Several studies have shown that the signal transducer and activator of transcription 3 (STAT3) is involved in the co-regulation of GFAP and VEGF. We show that STAT3 and βA3/A1-crystallin may co-regulate each other in astrocytes. Such co-regulation would create a positive feedback circuit; i.e., in the cytosol of astrocytes, βA3/A1-crystallin is necessary for the phosphorylation of STAT3, which then dimerizes and translocates to the nucleus to form DNA-binding complexes, activating transcription of Cryba1. This stoichiometric co-regulation of STAT3 and Cryba1 could potentiate expression of GFAP and secretion of VEGF, both of which are essential for maintaining astrocyte and blood vessel homeostasis in the retina. Consistent with this idea, Cryba1 knockout mice exhibit an abnormal astrocyte pattern and defective remodeling of retinal vessels.

Indexed as

Signal TransductionAnimalsAstrocytesBase Sequencebeta-Crystallin A ChainBinding SitesCrystallinsGene ExpressionImmunoblottingMice, KnockoutMicroscopy, ConfocalMolecular Sequence DataMutationOptic NervePhosphorylationPromoter Regions, GeneticbetaA3-crystallin, ratbeta-Crystallin A ChainCryba1 protein, mouseCrystallinsReceptors, NotchSTAT3 Transcription Factor

Identifiers

PMID25736717
PMCPMC4348628
OpenAlexW2021155213

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.