Evidence map›Paper›PMID 31997156›Full record

ArticleTranslational stroke research2020

Silencing of Long Non-coding RNA GAS5 Suppresses Neuron Cell Apoptosis and Nerve Injury in Ischemic Stroke Through Inhibiting DNMT3B-Dependent MAP4K4 Methylation.

Yiming Deng, Duanduan Chen, Feng Gao, Hong Lv, Guojun Zhang, Xuan Sun, Lian Liu, Dapeng Mo, Ning Ma, Ligang Song and 5 more

Abstract read
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In one paragraph

Article in Translational stroke research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  8. Mitochondrial Fragmentation and Long Noncoding RNAInternational journal of molecular sciences · 2025
    Article
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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

15 authors at 3 institutions in 1 country.

Yiming Deng *Department of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Duanduan Chen *School of Life Science, Beijing Institute of Technology, Beijing, 100081, People's Republic of China.
Feng GaoDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Hong LvDepartments of Clinical Laboratory, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Guojun ZhangDepartments of Clinical Laboratory, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Xuan SunDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Lian LiuDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Dapeng MoDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Ning MaDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Ligang SongDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Xiaochuan HuoDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Tianyi YanSchool of Life Science, Beijing Institute of Technology, Beijing, 100081, People's Republic of China.
Jingbo ZhangDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China.
Yun LuoDepartments of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, 210008, People's Republic of China. njluoyun@sina.com.
Zhongrong MiaoDepartment of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, People's Republic of China. zhongrongm@126.com.
Capital Medical University · CNBeijing Institute of Technology · CNNanjing Drum Tower Hospital · CN

Funding

Beijing Municipal Administration of Hospitals' Youth Program QML20180506Capital Medical University PYZ2018080National Natural Science Foundation of China 81671776, 81371290 and 81671140the National Key Research and Development Program of China 2016YFC1301501the Natural Science Foundation of Beijing 7172070
6 · The paper itself

Abstract

Ischemic stroke is associated with various physiological and pathological processes including neuronal apoptosis. Growth-arrest-specific transcript 5 (GAS5), a long non-coding RNA (lncRNA), has been recently reported to affect ischemic stroke-induced neuron apoptosis, while its mechanisms remain largely undefined. Through in silico analysis, GAS5 was predicted to interact with the promoter of MAP4K4. The aim of the present study was therefore to investigate the possible role of GAS5 in the progression of ischemic stroke via regulation of mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) methylation. The expression of MAP4K4 was found to be lowly expressed in the clinical samples collected from 55 patients. MAP4K4 was suggested to be methylated in an in vitro model of oxygen-glucose deprivation (OGD)-treated mouse primary cortical neurons, while its overexpression could inhibit OGD-induced neuronal apoptosis. A series of dual-luciferase reporter, RIP, RNA pull-down, ChIP MSP, and BSP assays confirmed that GAS5 significantly induced MAP4K4 methylation and downregulated MAP4K4 expression through the recruitment of DNA methyltransferase 3B (DNMT3B). An in vivo ischemic stroke model was developed using middle cerebral artery occlusion (MCAO). Upregulation of GAS5 promoted OGD-induced neuronal apoptosis in the in vitro model and increased cerebral infarction size and neurological score in the in vivo model by reducing MAP4K4 expression. Collectively, the present study highlights that silencing GAS5 may inhibit neuronal apoptosis and improve neurological function in ischemic stroke by suppressing DNMT3B-mediated MAP4K4 methylation, which contributes to better understanding of the pathologies of ischemic stroke and development of novel therapeutic options for this disease.

Indexed as

AdultAgedAnimalsApoptosisBrain IschemiaDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BFemaleHumansIntracellular Signaling Peptides and ProteinsIschemic StrokeMaleMethylationMice, Inbred C57BLMiddle AgedNeuronsDNA (Cytosine-5-)-MethyltransferasesDNA Methyltransferase 3BGAS5 long non-coding RNA, humanIntracellular Signaling Peptides and Proteinslong non-coding RNA GAS5, mouseMAP4K4 protein, humanProtein Serine-Threonine KinasesRNA, Long NoncodingApoptosisDNMT3BGAS5Ischemic strokeMAP4K4MethylationNeurological functionNeuron

Identifiers

PMID31997156
OpenAlexW3004251912

What OpenQuestion holds

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Registered trials

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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.