Evidence map›Paper›PMID 30102687›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2018

Micro-RNA-137 Inhibits Tau Hyperphosphorylation in Alzheimer's Disease and Targets the CACNA1C Gene in Transgenic Mice and Human Neuroblastoma SH-SY5Y Cells.

Yang Jiang, Bing Xu, Jing Chen, Yi Sui, Li Ren, Jing Li, Huiyu Zhang, Liqing Guo, Xiaohong Sun

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

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  12. The Role of miR-137 in Neurodegenerative Disorders.International journal of molecular sciences · 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 2 institutions in 1 country.

Yang JiangDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).
Bing XuDepartment of Neurology and Neuroscience, Shenyang First People's Hospital, Shenyang Brain Hospital, Shenyang Brain Institute, Shenyang, Liaoning, China (mainland).
Jing ChenDepartment of Neurology and Neuroscience, henyang Tenth People's Hospital, Shenyang Chest Hospital, Shenyang, Liaoning, China (mainland).
Yi SuiDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).
Li RenDepartment of Neurology and Neuroscience, Shenyang First People's Hospital, Shenyang Brain Hospital, Shenyang Brain Institute, Shenyang, Liaoning, China (mainland).
Jing LiDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).
Huiyu ZhangDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).
Liqing GuoDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).
Xiaohong SunDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning, China (mainland).
Fourth Affiliated Hospital of China Medical University · CNShenyang First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND Alzheimer's disease (AD) results in cognitive impairment. The calcium voltage-gated channel subunit alpha-1 C CACNA1C gene encodes an alpha-1 C subunit of L-type calcium channel (LTCC). The aim of this study was to investigate the role of micro-RNA-137 (miR-137) and the CACNA1C gene in APPswe/PS1ΔE9 (APP/PS1) double-transgenic AD mice and in human neuroblastoma SH-SY5Y cells. MATERIAL AND METHODS Six-month-old APP/PS1 double-transgenic AD mice (N=6) and age-matched normal C57BL/6 mice (N=6) underwent a Morris water maze (MWM) test, expression levels of amyloid-β (Aβ), LTCC, the CACNA1C gene, and miR-137 were measured in the rat hippocampus and cerebral cortex in both groups of mice. A luciferase assay was used to evaluate the effect of miR-137 on the expression of CACNA1C in SH-SY5Y human neuroblastoma SH-SY5Y cells. Western blotting was used to detect the CACNA1C, phosphorylated-tau (p-tau), and Aβ proteins. RESULTS In APP/PS1 transgenic AD mice, spatial learning and memory was significantly reduced, levels of Aβ1-40 and Aβ1-42 were increased in the serum, hippocampus, and cerebral cortex, expression levels of miR-137 were reduced, expression of CACNA1C protein was increased in the hippocampus and cerebral cortex, compared with normal control mice. miR-137 regulated the expression of the CACNA1C gene. Increased expression levels of p-tau (Ser202, Ser396, and Ser404) induced by Aβ1-42 were inhibited by miR-137 mimics in SH-SY5Y human neuroblastoma cells in vitro. CONCLUSIONS In a transgenic mouse model of AD, miR-137 and expression of the CACNA1C gene inhibited the hyperphosphorylation of tau protein.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsCalcium Channels, L-TypeCell Line, TumorCognitive DysfunctionDisease Models, AnimalGene Expression Regulation, NeoplasticHippocampusHumansMaleMiceMice, Inbred C57BLMice, TransgenicMicroRNAsAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorCACNA1C protein, humanCACNA1C protein, mouseCalcium Channels, L-TypeMAPT protein, humanMapt protein, mouseMicroRNAsMIRN137 microRNA, humanMIRN137 microRNA, mousePeptide Fragmentstau Proteins

Identifiers

PMID30102687
PMCPMC6104547
OpenAlexW2887651840

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.