Regulatory Mechanisms of Skeletal Muscle Stem/Progenitor Cells in Physiological and Pathological Conditions - Series 2

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

Deadline for manuscript submissions: closed (15 February 2022) | Viewed by 15794

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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
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Special Issue Information

Dear Colleagues,

Skeletal muscle stem/progenitor cells play essential roles in myogenesis, muscle repair, and homeostasis. In this Special Issue, we are collecting cutting-edge studies revealing the mechanisms by which the activation, proliferation, differentiation, self-renewal, and maintenance of muscle stem/progenitor cells are regulated in physiological and pathological conditions. It is especially fascinating to clarify the interaction between myogenic cells and their microenvironments. For example, non-myogenic cells, such as fibro-adipogenic precursors (FAPs) or inflammatory and immune cells, are usually indispensable for prompt muscle regeneration, but often aggravate diseases by promoting tissue damage, fibrosis, and adipocyte infiltration in pathological conditions. The factors that switch their phenotypes are still unclear. Genome-editing, direct reprogramming, and induced pluripotent stem (iPS) cells are also fascinating research fields that provide new therapeutic strategies for the cell-based treatment of muscle diseases. In this Special Issue, we hope to provide a place to exchange information, overview the field, and discuss future directions of research on muscle stem/progenitor cells.

Dr. Yuko Miyagoe-Suzuki
Guest Editor

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Keywords

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

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Published Papers (4 papers)

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Research

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11 pages, 1122 KiB  
Communication
Efficient Isolation of Lymphocytes and Myogenic Cells from the Tissue of Muscle Regeneration
by Yasuo Kitajima, Ryoka Tsukahara, Shohei Nakamoto and Tomoharu Yasuda
Cells 2022, 11(11), 1754; https://doi.org/10.3390/cells11111754 - 26 May 2022
Viewed by 3469
Abstract
Isolation of both lymphocytes and myogenic cells from muscle tissue is required for elucidating the cellular and molecular mechanisms of muscle regeneration. Here, we aimed to establish an optimal method obtaining a high yield of lymphocytes during muscle regeneration. After the muscle injury, [...] Read more.
Isolation of both lymphocytes and myogenic cells from muscle tissue is required for elucidating the cellular and molecular mechanisms of muscle regeneration. Here, we aimed to establish an optimal method obtaining a high yield of lymphocytes during muscle regeneration. After the muscle injury, we observed higher infiltration of lymphocytic cells in the muscle on day 3 after injury. Then, we compared two different white blood cell isolation methods, the Percoll gradient and CD45-magnetic bead methods, to assess the percentage and number of T and B cells. Flow cytometry analysis showed that the CD45-magnetic bead method has a better efficiency in isolating CD4+, CD8+ T cells, and B cells from injured muscle tissues of wild-type and mdx mice than that by the Percoll gradient method. Moreover, we found that the CD45-negative fraction from wild-type and mdx mice includes myogenic cells. In conclusion, we report that the CD45-magnetic bead method is suitable to isolate T and B cells during muscle regeneration with higher purity and yield and can also isolate myogenic cells within the same sample. This method provides a technical basis for further studies on muscle regeneration, involving lymphocytes and muscle cells, with a wide range of clinical applications. Full article
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14 pages, 3032 KiB  
Article
Inflammatory Caspase Activity Mediates HMGB1 Release and Differentiation in Myoblasts Affected by Peripheral Arterial Disease
by Ricardo Ferrari, Bowen Xie, Edwyn Assaf, Kristin Morder, Melanie Scott, Hong Liao, Michael J. Calderon, Mark Ross, Patricia Loughran, Simon C. Watkins, Iraklis Pipinos, George Casale, Edith Tzeng, Ryan McEnaney and Ulka Sachdev
Cells 2022, 11(7), 1163; https://doi.org/10.3390/cells11071163 - 30 Mar 2022
Cited by 2 | Viewed by 2490
Abstract
Introduction: We previously showed that caspase-1 and -11, which are activated by inflammasomes, mediate recovery from muscle ischemia in mice. We hypothesized that similar to murine models, inflammatory caspases modulate myogenicity and inflammation in ischemic muscle disease. Methods: Caspase activity was measured in [...] Read more.
Introduction: We previously showed that caspase-1 and -11, which are activated by inflammasomes, mediate recovery from muscle ischemia in mice. We hypothesized that similar to murine models, inflammatory caspases modulate myogenicity and inflammation in ischemic muscle disease. Methods: Caspase activity was measured in ischemic and perfused human myoblasts in response to the NLRP3 and AIM2 inflammasome agonists (nigericin and poly(dA:dT), respectively) with and without specific caspase-1 or pan-caspase inhibition. mRNA levels of myogenic markers and caspase-1 were assessed, and protein levels of caspases-1, -4, -5, and -3 were measured by Western blot. Results: When compared to perfused cells, ischemic myoblasts demonstrated attenuated MyoD and myogenin and elevated caspase-1 mRNA. Ischemic myoblasts also had significantly higher enzymatic caspase activity with poly(dA:dT) (p < 0.001), but not nigericin stimulation. Inhibition of caspase activity including caspase-4/-5, but not caspase-1, blocked activation effects of poly(dA:dT). Ischemic myoblasts had elevated cleaved caspase-5. Inhibition of caspase activity deterred differentiation in ischemic but not perfused myoblasts and reduced the release of HMGB1 from both groups. Conclusion: Inflammatory caspases can be activated in ischemic myoblasts by AIM2 and influence ischemic myoblast differentiation and release of pro-angiogenic HMGB1. AIM2 inflammasome involvement suggests a role as a DNA damage sensor, and our data suggest that caspase-5 rather than caspase-1 may mediate the downstream mediator of this pathway. Full article
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14 pages, 3498 KiB  
Article
Role of MiR-325-3p in the Regulation of CFL2 and Myogenic Differentiation of C2C12 Myoblasts
by Mai Thi Nguyen and Wan Lee
Cells 2021, 10(10), 2725; https://doi.org/10.3390/cells10102725 - 12 Oct 2021
Cited by 8 | Viewed by 3019
Abstract
Skeletal myogenesis is required to maintain muscle mass and integrity, and impaired myogenesis is causally linked to the etiology of muscle wasting. Recently, it was shown that excessive uptake of saturated fatty acids (SFA) plays a significant role in the pathogenesis of muscle [...] Read more.
Skeletal myogenesis is required to maintain muscle mass and integrity, and impaired myogenesis is causally linked to the etiology of muscle wasting. Recently, it was shown that excessive uptake of saturated fatty acids (SFA) plays a significant role in the pathogenesis of muscle wasting. Although microRNA (miRNA) is implicated in the regulation of myogenesis, the molecular mechanism whereby SFA-induced miRNAs impair myogenic differentiation remains largely unknown. Here, we investigated the regulatory roles of miR-325-3p on CFL2 expression and myogenic differentiation in C2C12 myoblasts. PA impeded myogenic differentiation, concomitantly suppressed CFL2 and induced miR-325-3p. Dual-luciferase analysis revealed that miR-325-3p directly targets the 3′UTR of CFL2, thereby suppressing the expression of CFL2, a crucial factor for actin dynamics. Transfection with miR-325-3p mimic resulted in the accumulation of actin filaments (F-actin) and nuclear Yes-associated protein (YAP) in myoblasts and promoted myoblast proliferation and cell cycle progression. Consequently, miR-325-3p mimic significantly attenuated the expressions of myogenic factors and thereby impaired the myogenic differentiation of myoblasts. The roles of miR-325-3p on CFL2 expression, F-actin modulation, and myogenic differentiation suggest a novel miRNA-mediated regulatory mechanism of myogenesis and PA-inducible miR-325-3p may be a critical mediator between obesity and muscle wasting. Full article
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Review

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14 pages, 1317 KiB  
Review
Factors Regulating or Regulated by Myogenic Regulatory Factors in Skeletal Muscle Stem Cells
by Tomohiko Shirakawa, Takashi Toyono, Asako Inoue, Takuma Matsubara, Tatsuo Kawamoto and Shoichiro Kokabu
Cells 2022, 11(9), 1493; https://doi.org/10.3390/cells11091493 - 29 Apr 2022
Cited by 35 | Viewed by 5998
Abstract
MyoD, Myf5, myogenin, and MRF4 (also known as Myf6 or herculin) are myogenic regulatory factors (MRFs). MRFs are regarded as master transcription factors that are upregulated during myogenesis and influence stem cells to differentiate into myogenic lineage cells. In this review, we summarize [...] Read more.
MyoD, Myf5, myogenin, and MRF4 (also known as Myf6 or herculin) are myogenic regulatory factors (MRFs). MRFs are regarded as master transcription factors that are upregulated during myogenesis and influence stem cells to differentiate into myogenic lineage cells. In this review, we summarize MRFs, their regulatory factors, such as TLE3, NF-κB, and MRF target genes, including non-myogenic genes such as taste receptors. Understanding the function of MRFs and the physiology or pathology of satellite cells will contribute to the development of cell therapy and drug discovery for muscle-related diseases. Full article
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