MicroRNA suppression of stress-responsive NDRG2 during dexamethasone treatment in skeletal muscle cells

Mir, Bilal Ahmad, Islam, Rabia, Kalanon, Ming, Russell, Aaron and Foletta, Victoria 2019, MicroRNA suppression of stress-responsive NDRG2 during dexamethasone treatment in skeletal muscle cells, BMC molecular and cell biology, vol. 20, no. 1, doi: 10.1186/s12860-019-0194-3.

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Title MicroRNA suppression of stress-responsive NDRG2 during dexamethasone treatment in skeletal muscle cells
Author(s) Mir, Bilal Ahmad
Islam, Rabia
Kalanon, Ming
Russell, AaronORCID iD for Russell, Aaron orcid.org/0000-0002-7323-9501
Foletta, VictoriaORCID iD for Foletta, Victoria orcid.org/0000-0002-5209-6134
Journal name BMC molecular and cell biology
Volume number 20
Issue number 1
Article ID 12
Total pages 11
Publisher BioMed Central
Place of publication London, Eng.
Publication date 2019-05-28
ISSN 2661-8850
Keyword(s) Dexamethasone
Luciferase reporter assay
Stress response
Science & Technology
Life Sciences & Biomedicine
Cell Biology
Summary BACKGROUND: MicroRNAs (miRNAs) are increasingly being identified as modulatory molecules for physiological and pathological processes in muscle. Here, we investigated whether miRNAs influenced the expression of the stress-responsive gene N-myc downstream-regulated gene 2 (Ndrg2) in skeletal muscle cells through the targeted degradation or translation inhibition of NDRG2 mRNA transcripts during basal or catabolic stress conditions. RESULTS: Three miRNAs, mmu-miR-23a-3p (miR-23a), mmu-miR-23b-3p (miR-23b) and mmu-miR-28-5p (miR-28), were identified using an in silico approach and confirmed to target the 3' untranslated region of the mouse Ndrg2 gene through luciferase reporter assays. However, miR-23a, -23b or -28 overexpression had no influence on NDRG2 mRNA or protein levels up to 48 h post treatment in mouse C2C12 myotubes under basal conditions. Interestingly, a compensatory decrease in the endogenous levels of the miRNAs in response to each other's overexpression was measured. Furthermore, dexamethasone, a catabolic stress agent that induces NDRG2 expression, decreased miR-23a and miR-23b endogenous levels at 24 h post treatment suggesting an interplay between these miRNAs and NDRG2 regulation under similar stress conditions. Accordingly, when overexpressed simultaneously, miR-23a, -23b and -28 attenuated the dexamethasone-induced increase of NDRG2 protein translation but did not affect Ndrg2 gene expression. CONCLUSION: These findings highlight modulatory and co-regulatory roles for miR-23a, -23b and -28 and their novel regulation of NDRG2 during stress conditions in muscle.
Language eng
DOI 10.1186/s12860-019-0194-3
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2019, The Authors
Persistent URL http://hdl.handle.net/10536/DRO/DU:30122379

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