Evidence map›Paper›PMID 32605607›Full record

ArticleTranslational neurodegeneration2020

Downregulated miR-18b-5p triggers apoptosis by inhibition of calcium signaling and neuronal cell differentiation in transgenic SOD1 (G93A) mice and SOD1 (G17S and G86S) ALS patients.

Ki Yoon Kim, Yu Ri Kim, Kyung Won Choi, Mijung Lee, Somyung Lee, Wooseok Im, Je-Young Shin, Jin Young Kim, Yoon Ho Hong, Manho Kim and 2 more

Open access · goldAbstract read
In one paragraph

Article in Translational neurodegeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
3.1field-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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Ki Yoon KimDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Yu Ri KimDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Kyung Won ChoiDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Mijung LeeDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Somyung LeeDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Wooseok ImDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Je-Young ShinDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Jin Young KimDivision of Mass Spectrometry Research, Korea Basic Science Institute, Daejun, South Korea.
Yoon Ho HongDepartment of Neurology, Seoul National University Seoul Metropolitan Government Boramae Medical Center, Seoul, South Korea.
Manho KimDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.
Jong-Il KimDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, South Korea.
Jung-Joon SungDepartment of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea. jjsaint@snu.ac.kr.
Seoul National University Hospital · KRSeoul National University · KRKorea Basic Science Institute · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroRNAs (miRNAs) are endogenous non-coding RNAs that regulate gene expression at the post-transcriptional level and are key modulators in neurodegenerative diseases. Overexpressed miRNAs play an important role in ALS; however, the pathogenic mechanisms of deregulated miRNAs are still unclear.

methodsWe aimed to assess the dysfunction of RNAs or miRNAs in fALS (SOD1 mutations). We compared the RNA-seq of subcellular fractions in NSC-34 WT (hSOD1) and MT (hSOD1 (G93A)) cells to find altered RNAs or miRNAs. We identified that Hif1α and Mef2c were upregulated, and Mctp1 and Rarb were downregulated in the cytoplasm of NSC-34 MT cells.

resultsSOD1 mutations decreased the level of miR-18b-5p. Induced Hif1α which is the target for miR-18b increased Mef2c expression as a transcription factor. Mef2c upregulated miR-206 as a transcription factor. Inhibition of Mctp1 and Rarb which are targets of miR-206 induces intracellular Ca

conclusionsOur data indicate that SOD1 mutation decreases miR-18b-5p, which sequentially regulates Hif1α, Mef2c, miR-206, Mctp1 and Rarb in fALS-linked SOD1 mutation. These results provide new insights into the downregulation of miR-18b-5p dependent pathogenic mechanisms of ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsApoptosisCalcium SignalingCell DifferentiationCell LineDown-RegulationHumansInduced Pluripotent Stem CellsMiceMice, TransgenicMicroRNAsNeuronsSuperoxide DismutaseSuperoxide Dismutase-1MicroRNAsMIRN18 microRNA, humanSOD1 G93A proteinSOD1 protein, humanSuperoxide DismutaseSuperoxide Dismutase-1Hif1αMctp1 and RarbMef2cmiRNAs

Identifiers

PMID32605607
PMCPMC7328278
OpenAlexW3038958603

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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.