Evidence map›Paper›PMID 25428621›Full record

ArticleMolecular neurobiology2016

Mdivi-1 Protects Against Ischemic Brain Injury via Elevating Extracellular Adenosine in a cAMP/CREB-CD39-Dependent Manner.

Mei Cui, Hongyan Ding, Fangzhe Chen, Yanxin Zhao, Qi Yang, Qiang Dong

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.0field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

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  20. New insights into targeting mitochondria in ischemic injury.Apoptosis : an international journal on programmed cell death · 2021
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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

6 authors at 3 institutions in 1 country.

Mei CuiDepartment of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, No. 12 Middle Wulumuqi Road, Shanghai, 200040, China. cuimei@fudan.edu.cn.
Hongyan DingDepartment of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, No. 12 Middle Wulumuqi Road, Shanghai, 200040, China.
Fangzhe ChenDepartment of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, No. 12 Middle Wulumuqi Road, Shanghai, 200040, China.
Yanxin ZhaoDepartment of Neurology, The 10th People's Hospital, Tongji University, Shanghai, China.
Qi YangDepartment of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, No. 12 Middle Wulumuqi Road, Shanghai, 200040, China.
Qiang DongDepartment of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, No. 12 Middle Wulumuqi Road, Shanghai, 200040, China. dong_qiang@fudan.edu.cn.
Fudan University · CNHuashan Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to examine whether the neuroprotective effects of Mdivi-1 are attributable to extracellular ATP and adenosine. Mdivi-1 was administered prior to or post middle cerebral artery occlusion (MCAO). The extracellular adenosine was measured by in vivo microdialysis and high-pressure liquid chromatography (HPLC) in MCAO mouse model. Western blot was done to determine the influence of Mdivi-1 on the expression of CD39 and CREB phosphorylation both in vivo and in the cultured astrocytes. Intracellular cAMP and protein kinase A (PKA) activity were detected in primary astrocytes. Results showed that Mdivi-1 significantly reduced infarct volume and neurological scores when administered either prior to or post MCAO. Interestingly, pretreatment with Mdivi-1 resulted in marked increase of extracellular adenosine and concomitant decrease in ATP. The expression of CD39, but not CD73, was upregulated by Mdivi-1, which was associated with the elevated phosphorylated cAMP response element-binding protein (CREB), a transcription factor potentially regulating CD39 expression. In primary astrocytes, Mdivi-1 treatment induced increases in intracellular cAMP, PKA activity and CREB phosphorylation, and PKA-specific inhibitor completely reversed Mdivi-1-induced CD39 expression. Our results demonstrate that Mdivi-1 protects against ischemic brain injury through increasing extracellular adenosine, a process involving elevated CD39 expression that is likely modulated by cAMP/PKA/CREB cascade. Figure Potential mechanisms by which Mdivi-1 mediates the neuroprotection on cerebral ischemic stroke. Results from the present study indicate that Mdivi-1 protects against ischemic brain injury through increasing extracellular adenosine, a process involving elevated CD39 expression that is likely modulated by the cAMP/PKA/CREB cascades.

Indexed as

AdenosineAdenosine TriphosphateAnimalsAntigens, CDApyraseAstrocytesBlood-Brain BarrierBrain IschemiaCells, CulturedCyclic AMPCyclic AMP Response Element-Binding ProteinDynaminsExtracellular SpaceHydrolysisMaleMice, Inbred C57BL3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAdenosineAdenosine TriphosphateAntigens, CDApyraseCD39 antigenCyclic AMPCyclic AMP Response Element-Binding ProteinDnm1l protein, mouseDynaminsNeuroprotective AgentsQuinazolinonesReceptor, Adenosine A1AdenosinecAMP response element-binding proteinCD39Cerebral ischemiaMdivi-1Regional cerebral blood flow

Identifiers

PMID25428621
OpenAlexW1966923900

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.