Myomir dysregulation and reactive oxygen species in aged human satellite cells

Abstract

Satellite cells that reside on the myofibre surface are crucial for the muscle homeostasis and regeneration. Aging goes along with a less effective regeneration of skeletal muscle tissue mainly due to the decreased myogenic capability of satellite cells. This phenomenon impedes proper maintenance and contributes to the age-associated decline in muscle mass, known as sarcopenia. The myogenic potential impairment does not depend on a reduced myogenic cell number, but mainly on their difficulty to complete a differentiation program. The unbalanced production of reactive oxygen species in elderly people could be responsible for skeletal muscle impairments. microRNAs are conserved post-transcriptional regulators implicated in numerous biological processes including adult myogenesis. Here, we measure the ROS level and analyze myomiR (miR-1, miR-133b and miR-206) expression in human myogenic precursors obtained from Vastus lateralis of elderly and young subjects to provide the molecular signature responsible for the differentiation impairment of elderly activated satellite cells.

Dietary resveratrol confers apoptotic resistance to oxidative stress in myoblasts

“…Aging is associated with high levels of muscle ROS in vivo , which may contribute to increased apoptosis and cell death and reduced myoblast differentiation leading to poor muscle repair [20]. High levels of ROS are associated with metabolic diseases like diabetes [16,20,36], which may contribute to the loss of myoblast function, increase myoblast cell death [33] and further exacerbate muscle repair in aging.…”

“…High levels of ROS are associated with metabolic diseases like diabetes [16,20,36], which may contribute to the loss of myoblast function, increase myoblast cell death [33] and further exacerbate muscle repair in aging. Fulle and colleagues [25] have demonstrated that a high percentage of the myogenic precursor cells from elderly muscles undergo apoptosis triggered by mitochondrial-associated caspase-9 and this appears to be closely linked to the high ROS levels that are found in aged muscles [20]. Thus, we predict that strategies to attenuate high ROS levels should reduce apoptosis in myoblasts and improve muscle differentiation/repair in aging and in other diseases that have elevated ROS levels.…”

Zeb2 Regulates Myogenic Differentiation in Pluripotent Stem Cells

“…The process of skeletal muscle differentiation is governed at least in part by miR-1, miR-206, and miR-133, which regulate the expression of MRF-encoding genes such as MyoD, Myogenin, and Mef2 [31]. Indeed, microRNAs are important regulators involved in the establishment and maintenance of skeletal muscle differentiation [22,[32][33][34]. For example, it was demonstrated that the expression of both miR-1 and miR-133 was enriched in striated muscle, and the differentiated myoblasts showed an elevated expression of miR-1 and miR-133 [32].…”

“…RNA was extracted with Purelink RNA Mini Kits (Invitrogen, Life Technologies, Waltham, MA, USA), and genomic DNA traces were removed with Turbo DNase (Invitrogen, Life Technologies, Waltham, MA, USA), following the manufacturer's instructions. A qRT-PCR was performed on mESCs as described in [34]. The values represent the mean ± SD of three independent experiments performed in triplicate.…”

Influência das proteínas de choque térmico na resposta regenerativa de músculos esqueléticos de camundongos idosos.

“…Os miRNAs conhecidos como músculo-especificos foram descritos como participantes principalmente dos processos de proliferação de células satélite, miogênese e hipertrofia muscular, são eles, miR-1, miR-133a, miR-133b, miR-206, miR-208b, miR-486 e miR-499, os quais estão presentes nos músculos esquelético e cardiaco (Di Filippo et al, 2016;Horak et al, 2016;Van Rooij et al, 2008). Além disso, diversos estudos têm relatado outros miRNAs envolvidos na miogênese, como por exemplo, miR-26 na diferenciação de mioblastos (Dey et al, 2012), miR-128 na inibição de proliferação de mioblastos (Motohashi et al, 2013), e miR-489 na manutenção do estado de quiescência das células satélite (Cheung et al, 2012).…”