Age‐related changes in miR‐143‐3p:Igfbp5 interactions affect muscle regeneration

Soriano‐Arroquia, Ana; McCormick, Rachel; Molloy, Andrew; McArdle, Anne; Goljanek‐Whysall, Katarzyna

doi:10.1111/acel.12442

Cited by 70 publications

(73 citation statements)

References 43 publications

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“…C2C12 cells were simultaneously treated with miR‐181a mimic or antagomiRs and treated with DMSO (control), CCCP, or bafilomycin A and imaged as described above. Images were obtained either using a Zeiss fluorescent upright microscope (Model Imager M1) couples with AxioCam MRm and AxioVision software 4.8 or with an Olympus Fluoview3000 Laser confocal microscope and analysed using ImageJ as described previously (Soriano‐Arroquia, McCormick, Molloy, McArdle, & Goljanek‐Whysall, 2016). Cytotoxicity and ATP generation were measured using mitochondrial ToxGlo assay (G8000) from Promega as per the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

miR‐181a regulates p62/SQSTM1, parkin, and protein DJ‐1 promoting mitochondrial dynamics in skeletal muscle aging

et al. 2020

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One of the key mechanisms underlying skeletal muscle functional deterioration during aging is disrupted mitochondrial dynamics. Regulation of mitochondrial dynamics is essential to maintain a healthy mitochondrial population and prevent the accumulation of damaged mitochondria; however, the regulatory mechanisms are poorly understood. We demonstrated loss of mitochondrial content and disrupted mitochondrial dynamics in muscle during aging concomitant with dysregulation of miR‐181a target interactions. Using functional approaches and mito‐QC assay, we have established that miR‐181a is an endogenous regulator of mitochondrial dynamics through concerted regulation of Park2, p62/SQSTM1, and DJ‐1 in vitro. Downregulation of miR‐181a with age was associated with an accumulation of autophagy‐related proteins and abnormal mitochondria. Restoring miR‐181a levels in old mice prevented accumulation of p62, DJ‐1, and PARK2, and improved mitochondrial quality and muscle function. These results provide physiological evidence for the potential of microRNA‐based interventions for age‐related muscle atrophy and of wider significance for diseases with disrupted mitochondrial dynamics.

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Section: Methodsmentioning

confidence: 99%

miR‐181a regulates p62/SQSTM1, parkin, and protein DJ‐1 promoting mitochondrial dynamics in skeletal muscle aging

et al. 2020

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“…In line with this, age‐related changes in miR‐143 have recently been shown to affect muscle regeneration in vitro (Soriano‐Arroquia et al . ).…”

Section: Muscle and Heart Mirnasmentioning

confidence: 97%

MicroRNAs in metabolism

et al. 2016

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MicroRNAs (miRNAs) have within the past decade emerged as key regulators of metabolic homoeostasis. Major tissues in intermediary metabolism important during development of the metabolic syndrome, such as β‐cells, liver, skeletal and heart muscle as well as adipose tissue, have all been shown to be affected by miRNAs. In the pancreatic β‐cell, a number of miRNAs are important in maintaining the balance between differentiation and proliferation (miR‐200 and miR‐29 families) and insulin exocytosis in the differentiated state is controlled by miR‐7, miR‐375 and miR‐335. MiR‐33a and MiR‐33b play crucial roles in cholesterol and lipid metabolism, whereas miR‐103 and miR‐107 regulates hepatic insulin sensitivity. In muscle tissue, a defined number of miRNAs (miR‐1, miR‐133, miR‐206) control myofibre type switch and induce myogenic differentiation programmes. Similarly, in adipose tissue, a defined number of miRNAs control white to brown adipocyte conversion or differentiation (miR‐365, miR‐133, miR‐455). The discovery of circulating miRNAs in exosomes emphasizes their importance as both endocrine signalling molecules and potentially disease markers. Their dysregulation in metabolic diseases, such as obesity, type 2 diabetes and atherosclerosis stresses their potential as therapeutic targets. This review emphasizes current ideas and controversies within miRNA research in metabolism.

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“…This allows for 40 - 70% transfection efficiency with gene/microRNA levels being up- or down-regulated within a physiological range ( Figure 4 ;22). …”

Section: Representative Resultsmentioning

confidence: 99%

“…The existence of geriatric and/or non-functional human MPCs has been demonstrated62022. However, no difference in the behavior of freshly isolated human MPCs has also been shown27.…”

Section: Discussionmentioning

confidence: 99%

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Soriano‐Arroquia¹,

Clegg²,

Molloy³

et al. 2017

JoVE

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Skeletal muscle homeostasis depends on muscle growth (hypertrophy), atrophy and regeneration. During ageing and in several diseases, muscle wasting occurs. Loss of muscle mass and function is associated with muscle fiber type atrophy, fiber type switching, defective muscle regeneration associated with dysfunction of satellite cells, muscle stem cells, and other pathophysiological processes. These changes are associated with changes in intracellular as well as local and systemic niches. In addition to most commonly used rodent models of muscle ageing, there is a need to study muscle homeostasis and wasting using human models, which due to ethical implications, consist predominantly of in vitro cultures. Despite the wide use of human Myogenic Progenitor Cells (MPCs) and primary myoblasts in myogenesis, there is limited data on using human primary myoblast and myotube cultures to study molecular mechanisms regulating different aspects of age-associated muscle wasting, aiding in the validation of mechanisms of ageing proposed in rodent muscle. The use of human MPCs, primary myoblasts and myotubes isolated from adult and aged people, provides a physiologically relevant model of molecular mechanisms of processes associated with muscle growth, atrophy and regeneration. Here we describe in detail a robust, inexpensive, reproducible and efficient protocol for the isolation and maintenance of human MPCs and their progeny — myoblasts and myotubes from human muscle samples using enzymatic digestion. Furthermore, we have determined the passage number at which primary myoblasts from adult and aged people undergo senescence in an in vitro culture. Finally, we show the ability to transfect these myoblasts and the ability to characterize their proliferative and differentiation capacity and propose their suitability for performing functional studies of molecular mechanisms of myogenesis and muscle wasting in vitro.

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Age‐related changes in miR‐143‐3p:Igfbp5 interactions affect muscle regeneration

Cited by 70 publications

References 43 publications

miR‐181a regulates p62/SQSTM1, parkin, and protein DJ‐1 promoting mitochondrial dynamics in skeletal muscle aging

miR‐181a regulates p62/SQSTM1, parkin, and protein DJ‐1 promoting mitochondrial dynamics in skeletal muscle aging

MicroRNAs in metabolism

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

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