Inflamma-miR-21 Negatively Regulates Myogenesis during Ageing

Borja-Gonzalez, Maria, Casas-Martinez, Jose C, McDonagh, Brian and Goljanek-Whysall, Katarzyna ORCID: 0000-0001-8166-8800 (2020) Inflamma-miR-21 Negatively Regulates Myogenesis during Ageing. ANTIOXIDANTS, 9 (4). E345-.

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Official URL: http://dx.doi.org/10.3390/antiox9040345

Abstract

Ageing is associated with disrupted redox signalling and increased circulating inflammatory cytokines. Skeletal muscle homeostasis depends on the balance between muscle hypertrophy, atrophy and regeneration, however during ageing this balance is disrupted. The molecular pathways underlying the age-related decline in muscle regenerative potential remain elusive. microRNAs are conserved robust gene expression regulators in all tissues including skeletal muscle. Here, we studied satellite cells from adult and old mice to demonstrate that inhibition of miR-21 in satellite cells from old mice improves myogenesis. We determined that increased levels of proinflammatory cytokines, TNFα and IL6, as well as H<sub>2</sub>O<sub>2</sub>, increased miR-21 expression in primary myoblasts, which in turn resulted in their decreased viability and myogenic potential. Inhibition of miR-21 function rescued the decreased size of myotubes following TNFα or IL6 treatment. Moreover, we demonstrated that miR-21 could inhibit myogenesis in vitro via regulating IL6R, PTEN and FOXO3 signalling. In summary, upregulation of miR-21 in satellite cells and muscle during ageing may occur in response to elevated levels of TNFα and IL6, within satellite cells or myofibrillar environment contributing to skeletal muscle ageing and potentially a disease-related decline in potential for muscle regeneration.

Item Type:	Article
Uncontrolled Keywords:	microRNA, muscle, aging, sarcopenia, cachexia, regeneration, miR-21, IL6, IL6R
Depositing User:	Symplectic Admin
Date Deposited:	13 Jul 2020 15:12
Last Modified:	26 Jan 2024 17:02
DOI:	10.3390/antiox9040345
Open Access URL:	https://doi.org/10.3390/antiox9040345
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/3093879