Evidence map›Paper›PMID 30365051›Full record

ArticleInternational journal of molecular medicine2019

Brain-derived neurotrophic factor inhibits hyperglycemia-induced apoptosis and downregulation of synaptic plasticity-related proteins in hippocampal neurons via the PI3K/Akt pathway.

Yuan Zhong, Yitong Zhu, Ting He, Wei Li, Qinjie Li, Ya Miao

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

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  20. BDNF Therapeutic Mechanisms in Neuropsychiatric Disorders.International journal of molecular sciences · 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

6 authors at 2 institutions in 1 country.

Yuan ZhongDepartment of Gerontology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Yitong ZhuDepartment of Gerontology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Ting HeDepartment of Gerontology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Wei LiDepartment of Gerontology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Qinjie LiDepartment of Gerontology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Ya MiaoDepartment of Gerontology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is not known whether brain‑derived neurotrophic factor (BDNF) protects hippocampal neurons from high glucose‑induced apoptosis and/or synaptic plasticity dysfunction. The present study aimed to assess whether BDNF exerted a neuroprotective effect in rat hippocampal neurons exposed to high glucose and examine the underlying mechanisms. The apoptosis of primary hippocampal neurons was assessed by Annexin V‑fluorescein isothiocyanate/propidium iodide staining. The mRNA and protein expression levels were measured by reverse transcription‑-quantitative polymerase chain reaction and western blot experiments, respectively. Synaptic plasticity was evaluated by the immunolocalization of synaptophysin (Syn). Exposure of the hippocampal neurons to high glucose (75 mM for 72 h) resulted in cell apoptosis, decreased mRNA and protein expression levels of three synaptic plasticity‑related proteins (Syn, Arc and cyclic AMP response element‑binding protein), and changes in the cellular distribution of Syn, indicating loss of synaptic density. These effects of high glucose were partially or completely reversed by prior administration of BDNF (50 ng/ml for 24 h). Pre‑treatment with wortmannin, a phosphatidylinositol‑3‑kinase (PI3K) inhibitor, suppressed the ability of BDNF to inhibit the effects of high glucose. In addition, BDNF significantly upregulated the tropomyosin‑related kinase B, its cognate receptor, Akt and phosphorylated Akt at the protein levels under high glucose conditions. In conclusion, high glucose induced apoptosis and downregulated synaptic plasticity‑related proteins in hippocampal neurons. These effects were reversed by BDNF via the PI3K/Akt signaling pathway.

Indexed as

AnimalsApoptosisBrain-Derived Neurotrophic FactorCells, CulturedDown-RegulationGlucoseHippocampusHyperglycemiaNerve Tissue ProteinsNeuronal PlasticityNeuronsPhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-aktRats, Sprague-DawleyRNA, MessengerBrain-Derived Neurotrophic FactorGlucoseNerve Tissue ProteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID30365051
PMCPMC6257855
OpenAlexW2895852567

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.