Evidence map›Paper›PMID 29595472›Full record

ArticleeLife2018

Mechanism and consequence of abnormal calcium homeostasis in Rett syndrome astrocytes.

Qiping Dong, Qing Liu, Ronghui Li, Anxin Wang, Qian Bu, Kuan Hong Wang, Qiang Chang

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  4. MeCP2 gene therapy ameliorates disease phenotype in mouse model for Pitt Hopkins syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    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

7 authors at 2 institutions in 1 country.

Qiping DongWaisman Center, University of Wisconsin-Madison, Madison, United States.
Qing LiuUnit on Neural Circuits and Adaptive Behaviors, National Institute of Mental Health, Bethesda, United States.
Ronghui LiWaisman Center, University of Wisconsin-Madison, Madison, United States.ORCID http://orcid.org/0000-0001-6329-5895
Anxin WangWaisman Center, University of Wisconsin-Madison, Madison, United States.
Qian BuWaisman Center, University of Wisconsin-Madison, Madison, United States.
Kuan Hong WangUnit on Neural Circuits and Adaptive Behaviors, National Institute of Mental Health, Bethesda, United States.ORCID http://orcid.org/0000-0002-2249-5417
Qiang ChangWaisman Center, University of Wisconsin-Madison, Madison, United States.ORCID http://orcid.org/0000-0002-7625-2170
University of Wisconsin–Madison · USNational Institute of Mental Health · US

Funding

Molecular and Cellular Mechanisms of Experience-Dependent Cortical ProcessingZIAMH002897 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI WANG, KUAN · 2009 to 2018
$12.9M
Waisman Intellectual and Developmental Disabilities Research Center Down Syndrome RegistryU54HD090256 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI MESSING, ALBEE · 2016 to 2020
$6.0M
In Vivo Function of Neuronal Activity-Induced MeCP2 phosphorylationR01HD064743 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI CHANG, QIANG · 2010 to 2021
$3.0M
Studying the glial contribution to RTT pathogenesis using patient-specific iPSCsR21NS081484 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI CHANG, QIANG · 2012 to 2013
$399k
Astrocyte dysfunction in Rett syndromeR56NS100024 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI CHANG, QIANG · 2017 to 2017
$383k
Intramural NIH HHS ZIA MH002897NICHD NIH HHS R01 HD064743NICHD NIH HHS R01HD064743NICHD NIH HHS U54 HD090256NICHD NIH HHS U54HD090256NIMH NIH HHS ZIAMH002897NINDS NIH HHS R21 NS081484NINDS NIH HHS R21NS081484NINDS NIH HHS R56 NS100024NINDS NIH HHS R56NS100024
6 · The paper itself

Abstract

Astrocytes play an important role in Rett syndrome (RTT) disease progression. Although the non-cell-autonomous effect of RTT astrocytes on neurons was documented, cell-autonomous phenotypes and mechanisms within RTT astrocytes are not well understood. We report that spontaneous calcium activity is abnormal in RTT astrocytes in vitro, in situ, and in vivo. Such abnormal calcium activity is mediated by calcium overload in the endoplasmic reticulum caused by abnormal store operated calcium entry, which is in part dependent on elevated expression of TRPC4. Furthermore, the abnormal calcium activity leads to excessive activation of extrasynaptic NMDA receptors (eNMDARs) on neighboring neurons and increased network excitability in

Indexed as

HomeostasisAnimalsAstrocytesCalciumEndoplasmic ReticulumMethyl-CpG-Binding Protein 2Mice, KnockoutReceptors, N-Methyl-D-AspartateRett SyndromeTRPC Cation ChannelsCalciumMecp2 protein, mouseMethyl-CpG-Binding Protein 2Receptors, N-Methyl-D-AspartateTRPC4 ion channelTRPC Cation Channelsastrocytescalciumdevelopmental biologyhumanMeCP2mouseRett syndromestem cells

Identifiers

PMID29595472
PMCPMC5902163
OpenAlexW2795153441

What OpenQuestion holds

Textmetadata
LicenceCC0
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.