Evidence map›Paper›PMID 27553862›Full record

ArticleMitochondrion2016

miR-29a differentially regulates cell survival in astrocytes from cornu ammonis 1 and dentate gyrus by targeting VDAC1.

Creed M Stary, Xiaoyun Sun, YiBing Ouyang, Le Li, Rona G Giffard

Open access · greenAbstract read
In one paragraph

Article in Mitochondrion, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

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  12. MicroRNAs in brain development and cerebrovascular pathophysiology.American journal of physiology. Cell physiology · 2019
    Review
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  15. Review
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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

5 authors at 3 institutions in 2 countries.

Creed M StaryDept. of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305-5117, USA. Electronic address: cstary@stanford.edu.
Xiaoyun SunDept. of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305-5117, USA.
YiBing OuyangDept. of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305-5117, USA.
Le LiDept. of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305-5117, USA; Department of Anesthesiology, Zhujiang Hospital, Southern Medical University, 253 Industrial Road, Guangzhou 510280, Guangdong Province, China.
Rona G GiffardDept. of Anesthesiology, Perioperative and Pain Medicine, Stanford University School of Medicine, Stanford, CA 94305-5117, USA.
Stanford University · USStanford Medicine · USZhujiang Hospital · CN

Funding

Astrocytes and Ischemic Brain InjuryR01NS053898 · NINDS · STANFORD UNIVERSITY · PI GIFFARD, RONA G · 2007 to 2016
$3.8M
Stress Proteins in Brain Cell InjuryR01NS084396 · NINDS · STANFORD UNIVERSITY · PI GIFFARD, RONA G · 2013 to 2017
$1.7M
Mitochondrial protection in post-stroke recoveryR01NS080177 · NINDS · STANFORD UNIVERSITY · PI GIFFARD, RONA G · 2013 to 2017
$1.7M
American Heart Association-American Stroke Association 14FTF19970029NINDS NIH HHS R01 NS053898NINDS NIH HHS R01 NS080177NINDS NIH HHS R01 NS084396
6 · The paper itself

Abstract

Neurons in the cornu ammonis 1 (CA1) region of the hippocampus are vulnerable to cerebral ischemia, while dentate gyrus (DG) neurons are more resistant. This effect is mediated by local astrocytes, and may reflect differences in subregional hippocampal expression of miR-29a. We investigated the role of miR-29a on survival of hippocampal astrocytes cultured selectively from CA1 and DG in response to glucose deprivation (GD). CA1 astrocytes exhibited more cell death and a greater decrease in miR-29a than DG astrocytes. A reciprocal change was observed in the mitochondrial voltage dependent cation channel-1 (VDAC1), a regulator of mitochondria and target of miR-29a. In CA1 astrocytes, increasing miR-29a decreased VDAC1 and improved cell survival, while knockdown of VDAC1 improved survival. Finally, the protective effect of miR-29a was eliminated by inhibition of miR-29a/VDAC1 binding. These findings suggest that the selective vulnerability of the CA1 to injury may be due in part to a limited miR-29a response in CA1 astrocytes, allowing a greater increase in VDAC1-mediated cellular dysfunction in CA1 astrocytes.

Indexed as

Gene Expression RegulationAnimalsAstrocytesCells, CulturedCell SurvivalDentate GyrusHippocampusMiceMicroRNAsVoltage-Dependent Anion Channel 1MicroRNAsMIRN29 microRNA, mouseVdac1 protein, mouseVoltage-Dependent Anion Channel 1BrainGliaGlucose deprivationHippocampusIschemiaMicroRNAMitochondriaStroke

Identifiers

PMID27553862
PMCPMC6082172
OpenAlexW2513476850

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.