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• W2569595597 abstract "Exosome-dependent intercellular communication is an emerging signaling mechanism involved in tissue repair and regeneration. Now in this issue of Cell Stem Cell, Fry et al., 2016Fry C.S. Kirby T.J. Kosmac K. McCarthy J.J. Peterson C.A. Cell Stem Cell. 2016; 20 (this issue): 56-69Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar show that muscle stem cells communicate with fibrogenic cells by exosomal trafficking of microRNA-206 to regulate extracellular matrix deposition and muscle tissue remodeling. Exosome-dependent intercellular communication is an emerging signaling mechanism involved in tissue repair and regeneration. Now in this issue of Cell Stem Cell, Fry et al., 2016Fry C.S. Kirby T.J. Kosmac K. McCarthy J.J. Peterson C.A. Cell Stem Cell. 2016; 20 (this issue): 56-69Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar show that muscle stem cells communicate with fibrogenic cells by exosomal trafficking of microRNA-206 to regulate extracellular matrix deposition and muscle tissue remodeling. Exosomes are small cell-secreted vesicles that can carry proteins, DNA, mRNA, and microRNAs (miRNA) as cargo. These cargos regulate normal biological functions such as tissue regeneration and patterning, and exosome dysregulation has been implicated in a wide range of pathological conditions such as cancers and neurodegenerative diseases (McGough and Vincent, 2016McGough I.J. Vincent J.P. Development. 2016; 143: 2482-2493Crossref PubMed Scopus (135) Google Scholar). miRNAs are small non-coding RNAs that direct post-transcriptional silencing of complementary mRNAs, representing a powerful regulatory mechanism controlling a variety of cellular functions in developing and adult normal or diseased tissues. In this issue of Cell Stem Cell, Fry et al., 2016Fry C.S. Kirby T.J. Kosmac K. McCarthy J.J. Peterson C.A. Cell Stem Cell. 2016; 20 (this issue): 56-69Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar highlight the importance of exosome-mediated communication during muscle remodeling and show that satellite cells can actively remodel their extracellular environment during muscle adaptation. Satellite cells are reserve stem cells in skeletal muscle that are activated in response to stimuli, such as myofiber injury and exercise, to mediate skeletal muscle growth, repair, and homeostasis. Upon activation, satellite cells give rise to myogenic progenitor cells (MPCs), which proliferate and fuse to form new muscle fibers. Several miRNAs have been implicated in satellite cell proliferation, fate determination, and muscle regeneration. For example, miR-206 is highly expressed during muscle regeneration and has been reported to promote stem cell differentiation (Chen et al., 2010Chen J.F. Tao Y. Li J. Deng Z. Yan Z. Xiao X. Wang D.Z. J. Cell Biol. 2010; 190: 867-879Crossref PubMed Scopus (455) Google Scholar, Yuasa et al., 2008Yuasa K. Hagiwara Y. Ando M. Nakamura A. Takeda S. Hijikata T. Cell Struct. Funct. 2008; 33: 163-169Crossref PubMed Scopus (124) Google Scholar). Subsequent studies showed that mir-206 is a physiological regulator of Pax3-mediated satellite cell differentiation (Boutet et al., 2012Boutet S.C. Cheung T.H. Quach N.L. Liu L. Prescott S.L. Edalati A. Iori K. Rando T.A. Cell Stem Cell. 2012; 10: 327-336Abstract Full Text Full Text PDF PubMed Scopus (112) Google Scholar), and its genetic deletion delayed skeletal muscle regeneration in acutely injured or chronic diseased muscle (Liu et al., 2012Liu N. Williams A.H. Maxeiner J.M. Bezprozvannaya S. Shelton J.M. Richardson J.A. Bassel-Duby R. Olson E.N. J. Clin. Invest. 2012; 122: 2054-2065Crossref PubMed Scopus (250) Google Scholar). However, there is also conflicting evidence suggesting that miR-206 might be dispensable for skeletal muscle survival and regeneration (Boettger et al., 2014Boettger T. Wüst S. Nolte H. Braun T. Skelet. Muscle. 2014; 4: 23Crossref PubMed Scopus (63) Google Scholar). In a previous study, the Peterson lab showed that genetic depletion of satellite cells results in an increase in muscle extracellular matrix (ECM) during mechanical-induced hypertrophy (Fry et al., 2014Fry C.S. Lee J.D. Jackson J.R. Kirby T.J. Stasko S.A. Liu H. Dupont-Versteegden E.E. McCarthy J.J. Peterson C.A. FASEB J. 2014; 28: 1654-1665Crossref PubMed Scopus (191) Google Scholar). This model involves the surgical removal of the gastrocnemius and soleus muscles (synergist ablation), causing functional overload of the remaining plantaris muscle. The satellite cells in the plantaris muscle show an increase in activation, proliferation, and fusion into myofibers, resulting in hypertrophy and revealing the potential of satellite cells to adapt in response to a major insult. These studies led to the hypothesis that MPCs actively secrete factors that regulate ECM gene expression in muscle fibroblasts with resulting ECM deposition. Of note, elevated collagen gene expression was independent of TGF-β signaling, which is thought to be the primary contributor of muscle fibrosis in muscular dystrophies. In the current study (Fry et al., 2016Fry C.S. Kirby T.J. Kosmac K. McCarthy J.J. Peterson C.A. Cell Stem Cell. 2016; 20 (this issue): 56-69Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar), the authors demonstrate that miRNAs packaged in exosomes are responsible for MPC-mediated regulation of muscle fibrogenic cell collagen production (Figure 1). To do this, they isolated primary MPCs from Pax7CreER/+;Dicerfl/fl (Pax7-Dicer) mice, in which miRNAs were specifically and conditionally depleted in satellite cells after tamoxifen treatment. Muscle fibrogenic cells incubated with Pax7-Dicer MPC-derived exosomes showed increased collagen mRNA and decreased miR-206 expression compared to control exosomes. The authors then showed that Rrbp1, a master regulator of collagen biosynthesis, is a specific miR-206 target in vitro, and culturing fibrogenic cells with MPC exosomes from which miR-206 had been depleted also increased collagen mRNA expression. To demonstrate the importance of MPC-derived exosomal miR-206 in regulating collagen expression in an in vivo mechanical overload context, the authors performed synergist ablation surgery on mice to induce hypertrophy. Using this model, they showed that the presence of satellite cells in the first week following mechanical overload is critical for proper muscle regeneration. Depleting satellite cells during this period caused significant decreases in miR-206 expression, with consequent increases in Rrbp1 expression and collagen deposition around muscle fibers. Satellite cells have previously been shown to be directly involved in the development of a fibrotic muscle environment (Alexakis et al., 2007Alexakis C. Partridge T. Bou-Gharios G. Am. J. Physiol. Cell Physiol. 2007; 293: C661-C669Crossref PubMed Scopus (132) Google Scholar). Conversely, the composition and mechanical properties of the ECM have been shown to regulate satellite cell activity and renewal (Gilbert et al., 2010Gilbert P.M. Havenstrite K.L. Magnusson K.E. Sacco A. Leonardi N.A. Kraft P. Nguyen N.K. Thrun S. Lutolf M.P. Blau H.M. Science. 2010; 329: 1078-1081Crossref PubMed Scopus (1181) Google Scholar). However, the mechanisms that connect these feedback loops were largely unknown. Thus, the present work of Fry et al., 2016Fry C.S. Kirby T.J. Kosmac K. McCarthy J.J. Peterson C.A. Cell Stem Cell. 2016; 20 (this issue): 56-69Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar reveals a novel mechanism for synergic regulation of the ECM by MPCs and fibrogenic cells during muscle remodeling. Although the clinical implications of these results are somewhat preliminary, the data suggest that depletion of satellite cells and, therefore, lack of mir-206 extruded from MPC exosomes to fibrogenic cells may be involved in pathogenic remodeling of the muscle ECM. These findings are highly relevant to muscle diseases such as Duchenne muscular dystrophy (DMD), in which the stem cell population becomes depleted and excessive fibrosis negatively impacts muscle regeneration and contraction. Accordingly, Liu et al., 2012Liu N. Williams A.H. Maxeiner J.M. Bezprozvannaya S. Shelton J.M. Richardson J.A. Bassel-Duby R. Olson E.N. J. Clin. Invest. 2012; 122: 2054-2065Crossref PubMed Scopus (250) Google Scholar reported that depletion of miR-206 exacerbated the dystrophic phenotype in the DMD mdx mouse model. Given that secretion of exosomes is thought to be regulated and to target specific cellular populations, these exosomal functions of miR-206 suggest discrete roles for other miRNAs or factors delivered via this system in skeletal muscle. In addition, if satellite cell-mediated ECM deposition is indeed independent of TGF-β-driven fibrogenesis, these findings unveil a new mechanism contributing to muscle fibrosis and a new aspect to the multifaceted pathogenesis of DMD. The response of skeletal muscle to insults is highly complex and involves a milieu of cell types and factors that contribute to muscle homeostasis and remodeling. Further studies to understand the many pathways implicated in this process will be required, but the findings of Fry et al., 2016Fry C.S. Kirby T.J. Kosmac K. McCarthy J.J. Peterson C.A. Cell Stem Cell. 2016; 20 (this issue): 56-69Abstract Full Text Full Text PDF PubMed Scopus (202) Google Scholar reveal an exciting new mechanism of intercellular communication between satellite cells and muscle fibrogenic cells to mediate skeletal muscle remodeling. Although there is debate regarding the significance of miR-206 in muscle homeostasis, this study also provides precedence for examining other exosome cargos in muscle stem cells and other populations. Exosomal miRNAs have already been shown to play an important role in the progression of cardiovascular disease and cancer, but the demonstration by Fry et al. of their involvement in muscle fibrosis opens new avenues to investigate pathogenesis and factors involved in muscle diseases. Myogenic Progenitor Cells Control Extracellular Matrix Production by Fibroblasts during Skeletal Muscle HypertrophyFry et al.Cell Stem CellNovember 10, 2016In BriefStem cells interact with the surrounding extracellular environment to facilitate tissue plasticity. Fry and colleagues report that skeletal muscle myogenic progenitor cells (MPCs) secrete exosomes containing miR-206, which regulates fibrogenic cell collagen expression through repression of Rrbp1. MPC-mediated regulation of the muscle extracellular environment is necessary during early myofiber growth. Full-Text PDF Open Archive" @default.
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• W2569595597 title "Exosomal Small Talk Carries Strong Messages from Muscle Stem Cells" @default.
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