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.


Journal

Translational neurodegeneration
ISSN: 2047-9158
Titre abrégé: Transl Neurodegener
Pays: England
ID NLM: 101591861

Informations de publication

Date de publication:
01 07 2020
Historique:
received: 22 05 2019
accepted: 01 06 2020
entrez: 2 7 2020
pubmed: 2 7 2020
medline: 20 7 2021
Statut: epublish

Résumé

MicroRNAs (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. We 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. SOD1 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 Our 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.

Sections du résumé

BACKGROUND
MicroRNAs (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.
METHODS
We 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.
RESULTS
SOD1 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
CONCLUSIONS
Our 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.

Identifiants

pubmed: 32605607
doi: 10.1186/s40035-020-00203-4
pii: 10.1186/s40035-020-00203-4
pmc: PMC7328278
doi:

Substances chimiques

MIRN18 microRNA, human 0
MicroRNAs 0
SOD1 protein, human 0
SOD1 G93A protein EC 1.15.1.1
Superoxide Dismutase EC 1.15.1.1
Superoxide Dismutase-1 EC 1.15.1.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

23

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Auteurs

Ki Yoon Kim (KY)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Yu Ri Kim (YR)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Kyung Won Choi (KW)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Mijung Lee (M)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Somyung Lee (S)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Wooseok Im (W)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Je-Young Shin (JY)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Jin Young Kim (JY)

Division of Mass Spectrometry Research, Korea Basic Science Institute, Daejun, South Korea.

Yoon Ho Hong (YH)

Department of Neurology, Seoul National University Seoul Metropolitan Government Boramae Medical Center, Seoul, South Korea.

Manho Kim (M)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea.

Jong-Il Kim (JI)

Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, South Korea.

Jung-Joon Sung (JJ)

Department of Neurology, Seoul National University Hospital 28 yongon-Dong, Chongno-gu, Seoul, 110-744, Republic of Korea. jjsaint@snu.ac.kr.

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Classifications MeSH