Inflamma-miR-21 Negatively Regulates Myogenesis during Ageing

Borja‐Gonzalez, Maria; Casas-Martinez, Jose C; Goljanek‐Whysall, Katarzyna

doi:10.3390/antiox9040345

Cited by 32 publications

(21 citation statements)

References 74 publications

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“…miR-21 is one of the most studied miRs related to cellular senescence and inflammaging [ 18 , 40 ], and we found that it increased in EA and OA WT mice, whereas its expression did not change in NLRP3 − ones. As recently confirmed, miR-21 levels increased in senescent human umbilical vein endothelial cells (HUVECs) [ 41 ], in circulating extracellular vesicles of older people [ 41 ], as well as in plasma of older patients with frailty [ 17 ], whereas low miR-21 expression is related to health aging [ 18 ]. The pro-inflammatory effect of miR-21 may result from its ability to promote the NF-κB signaling pathway and subsequent NLRP3 inflammasome activation, acting directly on Toll-like receptors (TLRs) and/or through targeting A20 [ 15 ] ( Figure 8 ).…”

Section: Discussionmentioning

confidence: 96%

“…The pro-inflammatory effect of miR-21 may result from its ability to promote the NF-κB signaling pathway and subsequent NLRP3 inflammasome activation, acting directly on Toll-like receptors (TLRs) and/or through targeting A20 [ 15 ] ( Figure 8 ). Increased levels of proinflammatory cytokines, such as TNF-α and IL-6, as well as ROS, induced miR-21 expression in primary myoblast cultures, contributing to defective muscle regeneration and resulting in muscle atrophy [ 41 ]. The positive correlation between miR-21 expression and pro-caspase-1 and pro-IL-1β here measured, supports miR-21 relationship with age-dependent inflammation and muscle damage in WT mice.…”

Section: Discussionmentioning

confidence: 99%

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The Impact of Melatonin and NLRP3 Inflammasome on the Expression of microRNAs in Aged Muscle

et al. 2021

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Muscular aging is a complex process and underlying physiological mechanisms are not fully clear. In recent years, the participation of the NF-kB pathway and the NLRP3 inflammasome in the chronic inflammation process that accompanies the skeletal muscle’s aging has been confirmed. microRNAs (miRs) form part of a gene regulatory machinery, and they control numerous biological processes including inflammatory pathways. In this work, we studied the expression of four miRs; three of them are considered as inflammatory-related miRs (miR-21, miR-146a, and miR-223), and miR-483, which is related to the regulation of melatonin synthesis, among other targets. To investigate the changes of miRs expression in muscle along aging, the impact of inflammation, and the role of melatonin in aged skeletal muscle, we used the gastrocnemius muscle of wild type (WT) and NLRP3-knockout (NLRP3−) mice of 3, 12, and 24 months-old, with and without melatonin supplementation. The expression of miRs and pro-caspase-1, caspase-3, pro-IL-1β, bax, bcl-2, and p53, was investigated by qRT-PCR analysis. Histological examination of the gastrocnemius muscle was also done. The results showed that age increased the expression of miR-21 (p < 0.01), miR-146a, and miR-223 (p < 0.05, for both miRs) in WT mice, whereas the 24-months-old mutant mice revealed decline of miR-21 and miR-223 (p < 0.05), compared to WT age. The lack of NLRP3 inflammasome also improved the skeletal muscle fibers arrangement and reduced the collagen deposits compared with WT muscle during aging. For the first time, we showed that melatonin significantly reduced the expression of miR-21, miR-146a, and miR-223 (p < 0.05 for all ones, and p < 0.01 for miR-21 at 24 months old) in aged WT mice, increased miR-223 in NLRP3− mice (p < 0.05), and induced miR-483 expression in both mice strains, this increase being significant at 24 months of age.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

The Impact of Melatonin and NLRP3 Inflammasome on the Expression of microRNAs in Aged Muscle

et al. 2021

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“…The expression of the anti-apoptosis gene Bcl-2 and mitochondrial marker Nd-1 was also initially upregulated when miR-21 was inhibited. 117 In summary, miR-21 and miR-29 can promote cancer-associated sarcopenia, mainly by inducing cell apoptosis via TLR7/8 signaling.…”

Section: Cancer-derived Exosomal Micrornas In Sarcopeniamentioning

confidence: 98%

Exosomal microRNAs in cancer-related sarcopenia: Tumor-derived exosomal microRNAs in muscle atrophy

et al. 2021

Exp Biol Med (Maywood)

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Cancer-associated sarcopenia is a complex metabolic syndrome marked by muscle mass wasting. Muscle wasting is a serious complication that is a primary contributor to cancer-related mortality. The underlying molecular mechanisms of cancer-associated sarcopenia have not been completely described to date. In general, evidence shows that the main pathophysiological alterations in sarcopenia are associated with the degradation of cellular components, an exceptional inflammatory secretome and mitochondrial dysfunction. Importantly, we highlight the prospect that several miRNAs carried by tumor-derived exosomes that have shown the ability to promote inflammatory secretion, activate catabolism, and even participate in the regulation of cellular degradation pathways can be delivered to and exert effects on muscle cells. In this review, we aim to describe the current knowledge about the functions of exosomal miRNAs in the induction of cancer-associated muscle wasting and propose potential treatment strategies.

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“…Inhibition of miR-21 in muscle satellite cells from elderly mice has been found to exert beneficial effects on myogenesis and could improve the decreased myotube size in vitro . 79 …”

Section: Ncrnas In Muscle Atrophy Induced By Agingmentioning

confidence: 99%

Non-coding RNA basis of muscle atrophy

Liu

Deng

Qiu

et al. 2021

Molecular Therapy - Nucleic Acids

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Muscle atrophy is a common complication of many chronic diseases including heart failure, cancer cachexia, aging, etc. Unhealthy habits and usage of hormones such as dexamethasone can also lead to muscle atrophy. However, the underlying mechanisms of muscle atrophy are not completely understood. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), play vital roles in muscle atrophy. This review mainly discusses the regulation of ncRNAs in muscle atrophy induced by various factors such as heart failure, cancer cachexia, aging, chronic obstructive pulmonary disease (COPD), peripheral nerve injury (PNI), chronic kidney disease (CKD), unhealthy habits, and usage of hormones; highlights the findings of ncRNAs as common regulators in multiple types of muscle atrophy; and summarizes current therapies and underlying mechanisms for muscle atrophy. This review will deepen the understanding of skeletal muscle biology and provide new strategies and insights into gene therapy for muscle atrophy.

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Inflamma-miR-21 Negatively Regulates Myogenesis during Ageing

Cited by 32 publications

References 74 publications

The Impact of Melatonin and NLRP3 Inflammasome on the Expression of microRNAs in Aged Muscle

The Impact of Melatonin and NLRP3 Inflammasome on the Expression of microRNAs in Aged Muscle

Exosomal microRNAs in cancer-related sarcopenia: Tumor-derived exosomal microRNAs in muscle atrophy

Non-coding RNA basis of muscle atrophy

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