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Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Stem Cells".

Deadline for manuscript submissions: closed (1 August 2019) | Viewed by 38478

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Special Issue Editor

Dr. Yuko Miyagoe-Suzuki

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Guest Editor

Department of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1, Ogawa-higashicho, Kodaira, Tokyo 187-8502, Japan
Interests: satellite cells; skeletal muscle; regeneration; myogenesis; Duchene muscular dystrophy; cell therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Skeletal muscle is an important tissue not only for force production, but also for metabolism. Muscle stem cells/progenitors play essential roles in myogenesis, muscle repair, and homeostasis. In this Special Issue, we have tried to collect edge-cutting studies revealing the functional roles of muscle stem cells/progenitors in the physiological and pathological (muscle atrophy, musclar distrophies, and so on) conditions of the developmental stage and postnatal life. We especially focus on the molecular mechanisms by which the proliferation, differentiation, and self-renewal of muscle stem cells/progenitors are regulated. It is also important to clarify the interaction between myogenic cells and non-myogeic cells, such as fibro-adipogenic precursors (FAPs), which promote muscle regeneration in healthy individuals. Importantly, their dysfunction is related to impaired muscle regeneration, resulting in fibrosis and adipocyte infiltration. Genome-editing, dirent reprogramming, and induced pluripotent stem (iPS) cells are also fascinating research fields that provide new therapeutic strategies for the treatment of muscle diseases. In this Special Issue, we would like to provide readers a place to exchange information and discuss future directions of research on muscle stem cells/progenitors.

Dr. Yuko Miyagoe-Suzuki
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

skeletal muscle
myogenesis
regeneration
cell therapy
muscular dystrophy
satellite cells
muscle stem cells
muscle progenitors
sarcopenia
atrophy
hypertrophy
aging

Published Papers (7 papers)

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Research

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20 pages, 5250 KiB

Open AccessArticle

PFN2a Suppresses C2C12 Myogenic Development by Inhibiting Proliferation and Promoting Apoptosis via the p53 Pathway

by Huaqin Li, Lianjie Hou, Yu Zhang, Fangyi Jiang, Yifan Zhu, Qing X. Li, Ching Yuan Hu and Chong Wang

Cells 2019, 8(9), 959; https://doi.org/10.3390/cells8090959 - 23 Aug 2019

Cited by 12 | Viewed by 6462

Abstract

Skeletal muscle plays a crucial role in physical activity and in regulating body energy and protein balance. Myoblast proliferation, differentiation, and apoptosis are indispensable processes for myoblast myogenesis. Profilin 2a (PFN2a) is a ubiquitous actin monomer-binding protein and promotes lung cancer growth and metastasis through suppressing the nuclear localization of histone deacetylase 1 (HDAC1). However, how PFN2a regulates myoblast myogenic development is still not clear. We constructed a C2C12 mouse myoblast cell line overexpressing PFN2a. The CRISPR/Cas9 system was used to study the function of PFN2a in C2C12 myogenic development. We find that PFN2a suppresses proliferation and promotes apoptosis and consequentially downregulates C2C12 myogenic development. The suppression of PFN2a also decreases the amount of HDAC1 in the nucleus and increases the protein level of p53 during C2C12 myogenic development. Therefore, we propose that PFN2a suppresses C2C12 myogenic development via the p53 pathway. Si-p53 (siRNA-p53) reverses the PFN2a inhibitory effect on C2C12 proliferation and the PFN2a promotion effect on C2C12 apoptosis, and then attenuates the suppression of PFN2a on myogenic differentiation. Our results expand understanding of PFN2a regulatory mechanisms in myogenic development and suggest potential therapeutic targets for muscle atrophy-related diseases. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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16 pages, 7497 KiB

Open AccessArticle

MiR-501-3p Forms a Feedback Loop with FOS, MDFI, and MyoD to Regulate C2C12 Myogenesis

by Lianjie Hou, Linhui Zhu, Huaqin Li, Fangyi Jiang, Lingbo Cao, Ching Yuan Hu and Chong Wang

Cells 2019, 8(6), 573; https://doi.org/10.3390/cells8060573 - 11 Jun 2019

Cited by 15 | Viewed by 3792

Abstract

Skeletal muscle plays an essential role in maintaining body energy homeostasis and body flexibility. Loss of muscle mass leads to slower wound healing and recovery from illness, physical disability, poor quality of life, and higher health care costs. So, it is critical for us to understand the mechanism of skeletal muscle myogenic differentiation for maintaining optimal health throughout life. miR-501-3p is a novel muscle-specific miRNA, and its regulation mechanism on myoblast myogenic differentiation is still not clear. We demonstrated that FOS was a direct target gene of miR-501-3p, and MyoD regulated miR-501-3p host gene Clcn5 through bioinformatics prediction. Our previous laboratory experiment found that MDFI overexpression promoted C2C12 myogenic differentiation and MyoD expression. The database also showed there is an FOS binding site in the MDFI promoter region. Therefore, we hypothesize that miR-501-3p formed a feedback loop with FOS, MDFI, and MyoD to regulate myoblast differentiation. To validate our hypothesis, we demonstrated miR-501-3p function in the proliferation and differentiation period of C2C12 cells by transfecting cells with miR-501-3p mimic and inhibitor. Then, we confirmed there is a direct regulatory relationship between miR-501-3p and FOS, MyoD and miR-501-3p, FOS and MDFI through QPCR, dual-luciferase reporter system, and ChIP experiments. Our results not only expand our understanding of the muscle myogenic development mechanism in which miRNA and genes participate in controlling skeletal muscle development, but also provide treatment strategies for skeletal muscle or metabolic-related diseases in the future. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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15 pages, 3354 KiB

Open AccessArticle

Overexpression of miR-29 Leads to Myopathy that Resemble Pathology of Ullrich Congenital Muscular Dystrophy

by Chuncheng Liu, Lei Li, Mengxu Ge, Lijie Gu, Meng Wang, Kuo Zhang, Yang Su, Yuying Zhang, Chang Liu, Miaomiao Lan, Yingying Yu, Tongtong Wang, Qiuyan Li, Yaofeng Zhao, Zhengquan Yu, Ning Li and Qingyong Meng

Cells 2019, 8(5), 459; https://doi.org/10.3390/cells8050459 - 15 May 2019

Cited by 10 | Viewed by 4009

Abstract

Ullrich congenital muscular dystrophy (UCMD) bring heavy burden to patients’ families and society. Because the incidence of this disease is very low, studies in patients are extremely limited. Animal models of this disease are indispensable. UCMD belongs to extracellular matrix-related diseases. However, the disease models constructed by knocking out some pathogenic genes of human, such as the Col6a1, Col6a2, or Col6a3 gene, of mice could not mimic UCMD. The purpose of this study is to construct a mouse model which can resemble the pathology of UCMD. miR-29 is closely related to extracellular matrix deposition of tissues and organs. To address this issue, we developed a mouse model for overexpression miR-29 using Tet-on system. In the muscle-specific miR-29ab1 cluster transgenic mice model, we found that mice exhibited dyskinesia, dyspnea, and spinal anomaly. The skeletal muscle was damaged and regenerated. At the same time, we clarify the molecular mechanism of the role of miR-29 in this process. Different from human, Col4a1 and Col4a2, target genes of miR-29, are the key pathogenic genes associating with these phenotypes. This mouse model simulates the human clinical and pathological characteristics of UCMD patients and is helpful for the subsequent research and treatment of UCMD. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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14 pages, 1971 KiB

Open AccessArticle

Dermatopontin in Skeletal Muscle Extracellular Matrix Regulates Myogenesis

by Taeyeon Kim, Khurshid Ahmad, Sibhghatulla Shaikh, Arif Tasleem Jan, Myung-Gi Seo, Eun Ju Lee and Inho Choi

Cells 2019, 8(4), 332; https://doi.org/10.3390/cells8040332 - 9 Apr 2019

Cited by 36 | Viewed by 5930

Abstract

Dermatopontin (DPT) is an extensively distributed non-collagenous component of the extracellular matrix predominantly found in the dermis of the skin, and consequently expressed in several tissues. In this study, we explored the role of DPT in myogenesis and perceived that it enhances the cell adhesion, reduces the cell proliferation and promotes the myoblast differentiation in C2C12 cells. Our results reveal an inhibitory effect with fibronectin (FN) in myoblast differentiation. We also observed that DPT and fibromodulin (FMOD) regulate positively to each other and promote myogenic differentiation. We further predicted the 3D structure of DPT, which is as yet unknown, and validated it using state-of-the-art in silico tools. Furthermore, we explored the in-silico protein-protein interaction between DPT-FMOD, DPT-FN, and FMOD-FN, and perceived that the interaction between FMOD-FN is more robust than DPT-FMOD and DPT-FN. Taken together, our findings have determined the role of DPT at different stages of the myogenic process. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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Review

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19 pages, 917 KiB

Open AccessReview

Functions and Regulatory Mechanisms of lncRNAs in Skeletal Myogenesis, Muscle Disease and Meat Production

by Shanshan Wang, Jianjun Jin, Zaiyan Xu and Bo Zuo

Cells 2019, 8(9), 1107; https://doi.org/10.3390/cells8091107 - 19 Sep 2019

Cited by 63 | Viewed by 5604

Abstract

Myogenesis is a complex biological process, and understanding the regulatory network of skeletal myogenesis will contribute to the treatment of human muscle related diseases and improvement of agricultural animal meat production. Long noncoding RNAs (lncRNAs) serve as regulators in gene expression networks, and participate in various biological processes. Recent studies have identified functional lncRNAs involved in skeletal muscle development and disease. These lncRNAs regulate the proliferation, differentiation, and fusion of myoblasts through multiple mechanisms, such as chromatin modification, transcription regulation, and microRNA sponge activity. In this review, we presented the latest advances regarding the functions and regulatory activities of lncRNAs involved in muscle development, muscle disease, and meat production. Moreover, challenges and future perspectives related to the identification of functional lncRNAs were also discussed. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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19 pages, 798 KiB

Open AccessReview

Potential Therapies Using Myogenic Stem Cells Combined with Bio-Engineering Approaches for Treatment of Muscular Dystrophies

by Norio Motohashi, Yuko Shimizu-Motohashi, Thomas C. Roberts and Yoshitsugu Aoki

Cells 2019, 8(9), 1066; https://doi.org/10.3390/cells8091066 - 11 Sep 2019

Cited by 12 | Viewed by 5455

Abstract

Muscular dystrophies (MDs) are a group of heterogeneous genetic disorders caused by mutations in the genes encoding the structural components of myofibres. The current state-of-the-art treatment is oligonucleotide-based gene therapy that restores disease-related protein. However, this therapeutic approach has limited efficacy and is unlikely to be curative. While the number of studies focused on cell transplantation therapy has increased in the recent years, this approach remains challenging due to multiple issues related to the efficacy of engrafted cells, source of myogenic cells, and systemic injections. Technical innovation has contributed to overcoming cell source challenges, and in recent studies, a combination of muscle resident stem cells and gene editing has shown promise as a novel approach. Furthermore, improvement of the muscular environment both in cultured donor cells and in recipient MD muscles may potentially facilitate cell engraftment. Artificial skeletal muscle generated by myogenic cells and muscle resident cells is an alternate approach that may enable the replacement of damaged tissues. Here, we review the current status of myogenic stem cell transplantation therapy, describe recent advances, and discuss the remaining obstacles that exist in the search for a cure for MD patients. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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15 pages, 1126 KiB

Open AccessReview

Non-Coding RNA Regulates the Myogenesis of Skeletal Muscle Satellite Cells, Injury Repair and Diseases

by Yue Zhao, Mingming Chen, Di Lian, Yan Li, Yao Li, Jiahao Wang, Shoulong Deng, Kun Yu and Zhengxing Lian

Cells 2019, 8(9), 988; https://doi.org/10.3390/cells8090988 - 27 Aug 2019

Cited by 60 | Viewed by 6550

Abstract

Skeletal muscle myogenesis and injury-induced muscle regeneration contribute to muscle formation and maintenance. As myogenic stem cells, skeletal muscle satellite cells have the ability to proliferate, differentiate and self-renew, and are involved in muscle formation and muscle injury repair. Accumulating evidence suggests that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), are widely involved in the regulation of gene expression during skeletal muscle myogenesis, and their abnormal expression is associated with a variety of muscle diseases. From the perspective of the molecular mechanism and mode of action of ncRNAs in myogenesis, this review aims to summarize the role of ncRNAs in skeletal muscle satellite cells’ myogenic differentiation and in muscle disease, and systematically analyze the mechanism of ncRNAs in skeletal muscle development. This work will systematically summarize the role of ncRNAs in myogenesis and provide reference targets for the treatment of various muscle diseases, such as muscle dystrophy, atrophy and aberrant hypertrophy. Full article

(This article belongs to the Special Issue Regulatory Mechanisms of Skeletal Muscle Stem Cells/Progenitors in Physiological and Pathological Conditions)

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