MiR-9-5p Regulates Genes Linked to Cerebral Calcification in the Osteogenic Differentiation Model and Induces Generalized Alteration in the Ion Channels.


Journal

Journal of molecular neuroscience : MN
ISSN: 1559-1166
Titre abrégé: J Mol Neurosci
Pays: United States
ID NLM: 9002991

Informations de publication

Date de publication:
Sep 2021
Historique:
received: 15 08 2018
accepted: 15 03 2021
pubmed: 28 5 2021
medline: 18 1 2022
entrez: 27 5 2021
Statut: ppublish

Résumé

MicroRNA-9 (miR-9) modulates gene expression and demonstrates high structural conservation and wide expression in the central nervous system. Bioinformatics analysis predicts almost 100 ion channels, membrane transporters and receptors, including genes linked to primary familial brain calcification (PFBC), as possible miR-9-5p targets. PFBC is a neurodegenerative disorder, characterized by bilateral and symmetrical calcifications in the brain, associated with motor and behavioral disturbances. In this work, we seek to study the influence of miR-9-5p in regulating genes involved in PFBC, in an osteogenic differentiation model with SaOs-2 cells. During the induced calcification process, solute carrier family 20 member 2 (SLC20A2) and platelet-derived growth factor receptor beta (PDGFRB) were downregulated, while platelet-derived growth factor beta (PDGFB) showed no significant changes. Significantly decreased levels of SLC20A2 and PDGFRB were caused by the presence of miR-9-5p, while PDGFB showed no regulation. We confirmed the findings using an miR-9-5p inhibitor and also probed the cells in electrophysiological analysis to assess whether such microRNA might affect a broader range of ion channels, membrane transporters and receptors. Our electrophysiological data show that an increase of the miR-9-5p in SaOs-2 cells decreased the density and amplitude of the output ionic currents, indicating that it may influence the activity, and perhaps the expression, of some ionic channels. Additional investigations should determine whether such an effect is specific to miR-9-5p, and whether it could be used, together with the miR-9-5p inhibitor, as a therapeutic or diagnostic tool.

Identifiants

pubmed: 34041689
doi: 10.1007/s12031-021-01830-w
pii: 10.1007/s12031-021-01830-w
doi:

Substances chimiques

MIRN92 microRNA, human 0
MicroRNAs 0
Proto-Oncogene Proteins c-sis 0
SLC20A2 protein, human 0
Sodium-Phosphate Cotransporter Proteins, Type III 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1897-1905

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Darlene Paiva Bezerra (DP)

Keizo Asami Laboratory, Federal University of Pernambuco, Recife, PE, Brazil.

Juliana Pereira de Aguiar (JP)

Department of Biophysics and Radiobiology, Federal University of Pernambuco, Recife, PE, Brazil.

Matthew Philip Keasey (MP)

Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.

Cláudio Gabriel Rodrigues (CG)

Department of Biophysics and Radiobiology, Federal University of Pernambuco, Recife, PE, Brazil.

João Ricardo Mendes de Oliveira (JRM)

Keizo Asami Laboratory, Federal University of Pernambuco, Recife, PE, Brazil. joao.ricardo@ufpe.br.
Neuropsychiatry Department, Federal University of Pernambuco, Recife, PE, Brazil. joao.ricardo@ufpe.br.

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