Evidence map›Paper›PMID 27443384›Full record

ArticleCellular and molecular neurobiology2017

PirB Overexpression Exacerbates Neuronal Apoptosis by Inhibiting TrkB and mTOR Phosphorylation After Oxygen and Glucose Deprivation Injury.

Zhao-Hua Zhao, Bin Deng, Hao Xu, Jun-Feng Zhang, Ya-Jing Mi, Xiang-Zhong Meng, Xing-Chun Gou, Li-Xian Xu

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2017. 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
0.8field-weighted citation impact, top 29% 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, 15 citations in OpenAlex.

  1. Immune receptors and aging brain.Bioscience reports · 2024
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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

8 authors at 2 institutions in 1 country.

Zhao-Hua ZhaoDepartment of Anesthesiology, College of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Bin DengDepartment of Anesthesiology, College of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Hao XuInstitute of Basic and Translational Medicine & School of Basic Medical Sciences, Xi'an Medical University, Xi'an, 710021, China.
Jun-Feng ZhangInstitute of Basic and Translational Medicine & School of Basic Medical Sciences, Xi'an Medical University, Xi'an, 710021, China.
Ya-Jing MiInstitute of Basic and Translational Medicine & School of Basic Medical Sciences, Xi'an Medical University, Xi'an, 710021, China.
Xiang-Zhong MengDepartment of Anesthesiology, College of Stomatology, Fourth Military Medical University, Xi'an, 710032, China.
Xing-Chun GouDepartment of Anesthesiology, College of Stomatology, Fourth Military Medical University, Xi'an, 710032, China. gouxingchun@189.cn.
Li-Xian XuDepartment of Anesthesiology, College of Stomatology, Fourth Military Medical University, Xi'an, 710032, China. lixianxu2015@hotmail.com.
Xi'an Medical University · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have proven that paired immunoglobulin-like receptor B (PirB) plays a crucial suppressant role in neurite outgrowth and neuronal plasticity after central nervous system injury. However, the role of PirB in neuronal survival after cerebral ischemic injury and its mechanisms remains unclear. In the present study, the role of PirB is investigated in the survival and apoptosis of cerebral cortical neurons in cultured primary after oxygen and glucose deprivation (OGD)-induced injury. The results have shown that rebarbative PirB exacerbates early neuron apoptosis and survival. PirB gene silencing remarkably decreases early apoptosis and promotes neuronal survival after OGD. The expression of bcl-2 markedly increased and the expression of bax significantly decreased in PirB RNAi-treated neurons, as compared with the control- and control RNAi-treated ones. Further, phosphorylated TrkB and mTOR levels are significantly downregulated in the damaged neurons. However, the PirB silencing markedly upregulates phosphorylated TrkB and mTOR levels in the neurons after the OGD. Taken together, the overexpression of PirB inhibits the neuronal survival through increased neuron apoptosis. Importantly, the inhibition of the phosphorylation of TrkB and mTOR may be one of its mechanisms.

Indexed as

ApoptosisAnimalsCell HypoxiaCells, CulturedCell SurvivalCerebral CortexDown-RegulationGlucoseMembrane GlycoproteinsNeuronsNeuroprotective AgentsOxygenPhosphorylationProtein-Tyrosine KinasesReceptors, ImmunologicReceptor, trkBGlucoseMembrane GlycoproteinsmTOR protein, mouseNeuroprotective AgentsNtrk2 protein, mouseOxygenPirb protein, mouseProtein-Tyrosine KinasesReceptors, ImmunologicReceptor, trkBTOR Serine-Threonine KinasesApoptosismTORNeuronal survivalOGDPirBTrkB

Identifiers

PMID27443384
PMCPMC11482055
OpenAlexW2503824253

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.