Evidence map›Paper›PMID 30618628›Full record

ArticleFrontiers in cellular neuroscience2018

TAT-Ngn2 Enhances Cognitive Function Recovery and Regulates Caspase-Dependent and Mitochondrial Apoptotic Pathways After Experimental Stroke.

Yu Zhao, Jinling Wang, Jiwei Du, Baixiang Li, Xingchun Gou, Jiannan Liu, Lichao Hou, Hanfei Sang, Bin Deng

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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  4. TPPU Downregulates Oxidative Stress Damage and Induces BDNF Expression in PC-12 Cells.Computational and mathematical methods in medicine · 2022
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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

9 authors at 5 institutions in 1 country.

Yu ZhaoDepartment of Hygienic Toxicology, Public Health College, Harbin Medical University, Harbin, China.
Jinling WangDepartment of Emergency, Zhongshan Hospital, Xiamen University, Xiamen, China.
Jiwei DuDepartment of Nursing, Xiang'an Hospital, Xiamen University, Xiamen, China.
Baixiang LiDepartment of Hygienic Toxicology, Public Health College, Harbin Medical University, Harbin, China.
Xingchun GouShaanxi Key Laboratory of Brain Disorders & Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, China.
Jiannan LiuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, China.
Lichao HouDepartment of Anesthesiology, Xiang'an Hospital, Xiamen University, Xiamen, China.
Hanfei SangDepartment of Anesthesiology, Xiang'an Hospital, Xiamen University, Xiamen, China.
Bin DengDepartment of Anesthesiology, Xiang'an Hospital, Xiamen University, Xiamen, China.
Xiamen University · CNHarbin Medical University · CNHeilongjiang Provincial Hospital · CNXi'an Medical University · CNZhongshan Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurogenin-2 (Ngn2) is a basic helix-loop-helix (bHLH) transcription factor that contributes to the identification and specification of neuronal fate during neurogenesis. In our previous study, we found that Ngn2 plays an important role in alleviating neuronal apoptosis, which may be viewed as an attractive candidate target for the treatment of cerebral ischemia. However, novel strategies require an understanding of the function and mechanism of Ngn2 in mature hippocampal neurons after global cerebral ischemic injury. Here, we found that the expression of Ngn2 decreased in the hippocampus after global cerebral ischemic injury in mice and in primary hippocampal neurons after oxygen glucose deprivation (OGD) injury. Then, transactivator of transcription (TAT)-Ngn2, which was constructed by fusing a TAT domain to Ngn2, was effectively transported and incorporated into hippocampal neurons after intraperitoneal (i.p.) injection and enhanced cognitive functional recovery in the acute stage after reperfusion. Furthermore, TAT-Ngn2 alleviated hippocampal neuronal damage and apoptosis, and inhibited the cytochrome C (CytC) leak from the mitochondria to the cytoplasm through regulating the expression levels of brain-derived neurotrophic factor (BDNF), phosphorylation tropomyosin-related kinase B (pTrkB), Bcl-2, Bax and cleaved caspase-3 after reperfusion injury

Indexed as

apoptosisbrain-derived neurotrophic factorglobal cerebral ischemianeurogenin-2transactivator of transcription domain

Identifiers

PMID30618628
PMCPMC6302814
OpenAlexW2903832269

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.