Evidence map›Paper›PMID 32648620›Full record

ArticleJournal of cellular and molecular medicine2020

The overexpression of RBM3 alleviates TBI-induced behaviour impairment and AD-like tauopathy in mice.

Bingjin Liu, Yun Cao, Fangxiao Shi, Lin Wang, Na Li, Xiangshu Cheng, Jin Du, Qing Tian, Xinwen Zhou

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  6. Bmal1 integrates circadian function and temperature sensing in the suprachiasmatic nucleus.Proceedings of the National Academy of Sciences of the United States of America · 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

9 authors at 3 institutions in 1 country.

Bingjin LiuDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yun CaoDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fangxiao ShiDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Lin WangDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Na LiDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiangshu ChengDepartment of Neurology, Center for Translational Medicine, Huaihe Hospital of Henan University, Kaifeng, China.
Jin DuDepartment of Neurology, Center for Translational Medicine, Huaihe Hospital of Henan University, Kaifeng, China.
Qing TianDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xinwen ZhouDepartment of Pathophysiology, Key Laboratory of Neurological Diseases of Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0003-1357-7039
Huazhong University of Science and Technology · CNHenan University Huaihe Hospital and Huaihe Clinical Institute · CNTaizhou Vocational and Technical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The therapeutic hypothermia is an effective tool for TBI-associated brain impairment, but its side effects limit in clinical routine use. Hypothermia up-regulates RNA-binding motif protein 3 (RBM3), which is verified to protect synaptic plasticity. Here, we found that cognitive and LTP deficits, loss of spines, AD-like tau pathologies are displayed one month after TBI in mice. In contrast, the deficits of LTP and cognitive, loss of spines and tau abnormal phosphorylation at several sites are obviously reversed in TBI mice combined with hypothermia pre-treatment (HT). But, the neuroprotective role of HT disappears in TBI mouse models under condition of blocking RBM3 expression with RBM3 shRNA. In other hand, overexpressing RBM3 by AAV-RBM3 plasmid can mimic HT-like neuroprotection against TBI-induced chronic brain injuries, such as improving LTP and cognitive, loss of spines and tau hyperphosphorylation in TBI mouse models. Taken together, hypothermia pre-treatment reverses TBI-induced chronic AD-like pathology and behaviour deficits in RBM3 expression dependent manner, RBM3 may be a potential target for neurodegeneration diseases including Alzheimer disease.

Indexed as

Behavior, AnimalNeuroprotective AgentsAlzheimer DiseaseAnimalsBrain Injuries, TraumaticHypothermia, InducedMaleMiceMice, Inbred C57BLRNA-Binding ProteinsTauopathiesNeuroprotective AgentsRbm3 protein, mouseRNA-Binding Proteinscognitive deficitshypothermia pre-treatmentRNA-binding motif protein 3tau phosphorylationtraumatic brain injury

Identifiers

PMID32648620
PMCPMC7417709
OpenAlexW3042069202

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.