Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Public Library of Science (PLoS)  

Myogenic stem cells are a promising avenue for the treatment of muscular disorders. Freshly isolated muscle stem cells have a remarkable engraftment ability in vivo, but their cell number is limited. Current conventional culture conditions do not allow muscle stem cells to expand in vitro with their bona fide engraftment efficiency, requiring the improvement of culture procedures for achieving successful cell-therapy for muscle disorders. Here we expanded mouse muscle stem cells and human myoblasts with Notch ligands, DLL1, DLL4, and JAG1 to activate Notch signaling in vitro and to investigate whether these cells could retain their engraftment efficiency. Notch signaling promotes the expansion of Pax7+MyoD- mouse muscle stem-like cells and inhibits differentiation even after passage in vitro. Treatment with Notch ligands induced the Notch target genes and generated PAX7+MYOD- stem-like cells from human myoblasts previously cultured on conventional culture plates. However, cells treated with Notch ligands exhibit a stem cell-like state in culture, yet their regenerative ability was less than that of freshly isolated cells in vivo and was comparable to that of the control. These unexpected findings suggest that artificial maintenance of Notch signaling alone is insufficient for improving regenerative capacity of mouse and human donor-muscle cells and suggest that combinatorial events are critical to achieve muscle stem cell and myoblast engraftment potential.

File： file-2.pdf

DOI： 10.1371/journal.pone.0177516

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Public Library of Science (PLoS)  

File： Sakai_Sehara-Fujisawa_2013.pdf

DOI： 10.1371/journal.pone.0063016

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Language：English   Publishing type：Research paper (scientific journal)  

Androgen is widely acknowledged to regulate skeletal muscle mass, however, the specific mechanism driving muscle atrophy resulting from androgen deficiency remains elusive. Systemic androgen receptor knockout (ARKO) mice exhibit reduction in both muscle strength and muscle mass while skeletal muscle fiber specific ARKO mice have decreased muscle strength without affecting skeletal muscle mass in the limbs. Therefore, androgens may indirectly regulate skeletal muscle mass through effects on non-myofibers. Considering this, we investigated focusing on blood fluid factors that might play a role in the regulation of skeletal muscle mass under the influence of androgens. Using male mice model of sham, orchidectomy and DHT replacement, mass spectrometry for serum samples of each group identified epidermal growth factor receptor (EGFR) as a candidate protein involving the regulation of skeletal muscle mass affected by androgens. Egfr expression in both liver and epididymal white adipose tissue correlated with androgen levels. Furthermore, Egfr expression in these tissues was predominantly elevated in male compared to female mice. Interestingly, male mice exhibited significantly elevated serum EGFR concentrations compared to their female counterparts, suggesting a connection with androgen levels. Treatment of EGFR to C2C12 cells promoted phosphorylation of AKT and its downstream S6K, and enhanced the protein synthesis in vitro. Furthermore, the administration of EGFR to female mice revealed a potential role in promoting an increase in skeletal muscle mass. These findings collectively enhance our understanding of the complex interplay among androgens, EGFR, and the regulation of skeletal muscle mass.

DOI： 10.1507/endocrj.EJ24-0410

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Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.isci.2021.102303

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Wiley  

DOI： 10.1002/rco2.28

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Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/rco2.28

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

Epigenetic transcriptional regulation is essential for the differentiation of various types of cells, including skeletal muscle cells. DNA methyltransferase 1 (Dnmt1) is responsible for maintenance of DNA methylation patterns via cell division. Here, we investigated the relationship between Dnmt1 and skeletal muscle regeneration. We found that Dnmt1 is upregulated in muscles during regeneration. To assess the role of Dnmt1 in satellite cells during regeneration, we performed conditional knockout (cKO) of Dnmt1 specifically in skeletal muscle satellite cells using Pax7CreERT2 mice and Dnmt1 flox mice. Muscle weight and the cross-sectional area after injury were significantly lower in Dnmt1 cKO mice than in control mice. RNA sequencing analysis revealed upregulation of genes involved in cell adhesion and apoptosis in satellite cells from cKO mice. Moreover, satellite cells cultured from cKO mice exhibited a reduced number of cells. These results suggest that Dnmt1 is an essential factor for muscle regeneration and is involved in positive regulation of satellite cell number.

DOI： 10.1016/j.bbrc.2020.11.116

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：The Company of Biologists  

Pax7 expression marks stem cells in developing skeletal muscles and adult satellite cells during homeostasis and muscle regeneration. The genetic determinants that control the entrance into the myogenic program and the appearance of PAX7+ cells during embryogenesis are poorly understood. SIX homeoproteins are encoded by the Sine oculis homeobox related Six1-Six6 genes in vertebrates. Six1, Six2, Six4 and Six5 are expressed in the muscle lineage. Here we tested the hypothesis that Six1 and Six4 could participate in the genesis of myogenic stem cells. We show that fewer PAX7+ cells occupy a satellite cell position between the myofiber and its associated basal lamina in Six1 and Six4 (s1s4KO) at E18. However, PAX7+ cells are detected in remaining muscle masses present in the epaxial region of the double mutant embryos and are able to divide and contribute to muscle growth. To further characterize the properties of s1s4KO PAX7+ cells, we analyzed their transcriptome and tested their properties after transplantation in adult regenerating tibialis anterior (TA) muscle. Mutant stem cells form hypotrophic myofibers that are not innervated but retain the ability to self-renew.

DOI： 10.1242/dev.185975

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Other Link： http://journals.biologists.com/dev/article-pdf/doi/10.1242/dev.185975/1968029/dev185975.pdf

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.molcel.2019.02.026

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.stemcr.2019.01.007

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

DOI： 10.1186/s13287-017-0556-8

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Language：English   Publishing type：Part of collection (book)   Publisher：Springer New York  

DOI： 10.1007/978-1-4939-6771-1_2

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.stem.2016.11.020

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

DOI： 10.15252/embj.201489923

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Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.15252/embj.201489923

Language：English   Publishing type：Research paper (scientific journal)   Publisher：Elsevier BV  

DOI： 10.1016/j.mod.2014.12.001

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：Public Library of Science (PLoS)  

DOI： 10.1371/journal.pone.0047078

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Event date： 2024.11

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Fukuoka   Country：Japan  

Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via nonmyofiber cells. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with cell death and extracellular matrix organization. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1 (Igf1) and that IGF1 administration prevents perineal muscle atrophy in a paracrine manner. These findings indicate that the anabolic effects of androgens regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.

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Event date： 2024.11

Language：English   Presentation type：Poster presentation  

Venue：Matsuyama   Country：Japan  

Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via nonmyofiber cells. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with cell death and extracellular matrix organization. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1 (Igf1) and that IGF1 administration prevents perineal muscle atrophy in a paracrine manner. These findings indicate that the anabolic effects of androgens regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.

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Event date： 2024.9

Language：English   Presentation type：Oral presentation (general)  

Venue：Nara   Country：Japan  

Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via extra-myofiber cells or tissues. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with apoptosis and extracellular matrix organization. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1, which can increase skeletal muscle mass in a paracrine manner. These findings indicate that the anabolic effects of androgens regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.

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Event date： 2024.6

Language：English   Presentation type：Poster presentation  

Venue：Florida   Country：United States  

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Event date： 2024.5

Language：English   Presentation type：Poster presentation  

Venue：Tokyo   Country：Japan  

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Event date： 2024.3

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Sapporo   Country：Japan  

Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via extra-myofiber cells or tissues. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with apoptosis and proteolysis. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1, which can increase skeletal muscle mass in a paracrine manner. These findings indicate that the anabolic effects of androgens indirectly regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.

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Event date： 2024.2

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Tokyo   Country：Japan  

Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via extra-myofiber cells or tissues. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with apoptosis and proteolysis. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1, which can increase skeletal muscle mass in a paracrine manner. These findings indicate that the anabolic effects of androgens indirectly regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.

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Event date： 2023.9

Language：English   Presentation type：Poster presentation  

Venue：Ehime   Country：Japan  

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Event date： 2023.8

Language：English   Presentation type：Poster presentation  

Venue：Osaka   Country：Japan  

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Event date： 2023.8

Language：Japanese  

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Event date： 2023.3

Language：English   Presentation type：Oral presentation (general)  

Venue：Shonan   Country：Japan  

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Event date： 2023.2

Language：English   Presentation type：Oral presentation (general)  

Venue：Online  

Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via extra-myofiber cells or tissues. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with apoptosis and proteolysis. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1, which can increase skeletal muscle mass in a paracrine manner. These findings indicate that the anabolic effects of androgens indirectly regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.

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Event date： 2022.9

Language：English   Presentation type：Poster presentation  

Venue：Matsuyama   Country：Japan  

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Event date： 2022.8

Language：English   Presentation type：Oral presentation (general)  

Venue：Tokyo   Country：Japan  

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Event date： 2022.2

Language：English   Presentation type：Oral presentation (general)  

Venue：Online  

Androgens are biologically active compounds that bind to androgen receptors (AR) to mediate various effects, including muscle growth. While it's known that AR activation enhances muscle strength, the specific roles of AR in muscle cells remain unclear. My research aims to determine which cells in skeletal muscle are targeted by androgens/AR and how AR regulates their functions. Skeletal muscle is primarily composed of muscle cells, but also includes satellite cells (muscle stem cells) and mesenchymal progenitors, both of which express AR.
In previous studies, I found that inactivating AR in satellite cells does not affect muscle regeneration, suggesting that AR is not essential for this process. However, AR in muscle cells increases muscle strength by upregulating the Mylk4 gene. My current project focuses on mesenchymal progenitors, which also express AR. I have developed AR knockout mice to investigate how AR inactivation affects muscle function and gene regulation across muscle cells, satellite cells, and mesenchymal progenitors. This research aims to uncover new insights into AR's role in muscle biology.

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Event date： 2022

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Event date： 2022

Presentation type：Poster presentation  

Venue：東京   Country：Japan  

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Event date： 2021.12

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Kyoto   Country：Japan  

DNA methylation is an essential form of epigenetic regulation responsible for cellular identity. In muscle satellite cells, DNA methylation patterns are tightly regulated during differentiation. However, it is unclear how these DNA methylation patterns are maintained. We demonstrate that ubiquitin like with PHD and RING finger domains 1 (Uhrf1) is activated in proliferating myogenic cells. Ablation of Uhrf1 in satellite cells impairs their proliferation and differentiation, leading to failed muscle regeneration. Uhrf1-deficient satellite cells exhibited dramatic changes in genome-wide DNA methylation profiles and transcript levels. These findings point to Uhrf1 as a regulator of self-renewal and differentiation of satellite cells via genome-wide DNA methylation patterning.

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Event date： 2021.9

Language：Japanese   Presentation type：Oral presentation (general)  

Venue：Online  

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Event date： 2021.9

Language：English   Presentation type：Poster presentation  

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Event date： 2021.7

Language：English   Presentation type：Poster presentation  

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Event date： 2021.3

Language：English  

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Event date： 2021.3

Language：Japanese   Presentation type：Oral presentation (general)  

DNA methylation is an essential form of epigenetic regulation responsible for cellular identity. In muscle satellite cells, DNA methylation patterns are tightly regulated during differentiation. However, it is unclear how these DNA methylation patterns are maintained. We demonstrate that ubiquitin like with PHD and RING finger domains 1 (Uhrf1) is activated in proliferating myogenic cells. Ablation of Uhrf1 in satellite cells impairs their proliferation and differentiation, leading to failed muscle regeneration. Uhrf1-deficient satellite cells exhibited dramatic changes in genome-wide DNA methylation profiles and transcript levels. These findings point to Uhrf1 as a regulator of self-renewal and differentiation of satellite cells via genome-wide DNA methylation patterning.

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Event date： 2020.12

Language：English   Presentation type：Poster presentation  

Country：Japan  

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Event date： 2019.10

Language：English   Presentation type：Poster presentation  

Country：Japan  

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Event date： 2019.9

Language：English   Presentation type：Poster presentation  

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Event date： 2019.8

Language：English   Presentation type：Poster presentation  

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Event date： 2019.8

Language：Japanese  

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Event date： 2019.3

Language：English   Presentation type：Poster presentation  

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Event date： 2018.11

Presentation type：Poster presentation  

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Event date： 2018.11

Presentation type：Oral presentation (general)  

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Event date： 2018.8

Language：English   Presentation type：Poster presentation  

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Event date： 2017.1

Language：English   Presentation type：Poster presentation  

Venue：Chantilly-Gouvieux   Country：France  

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Event date： 2016.5

Language：English   Presentation type：Poster presentation  

Venue：Paris   Country：France  

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Event date： 2016.3

Language：English   Presentation type：Poster presentation  

Venue：Lyon   Country：France  

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Event date： 2016.2

Language：English   Presentation type：Poster presentation  

Venue：Chantilly-Gouvieux   Country：France  

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Event date： 2015.1

Language：English   Presentation type：Oral presentation (general)  

Venue：Belle-Eglise   Country：France  

Cell therapies for treating myopathic diseases with healthy donor cells have been proposed. Although satellite cells, which are mononuclear skeletal muscle stem cells and have the ability to self-renew and form new muscle fibers, are strong candidates for cell therapy as determined by studies with mice, human satellite cells are considerably less well understood. To qualify and expand mouse and human satellite cells, we transplanted them into the muscle of immunodeficient Pax7DTR/+:Rag2–/–:C–/– mice [1], in which endogenous mouse Pax7+ satellite cells can be depleted by the injection of diphtheria toxin. Upon transplantation, human satellite cells contribute to new muscle formation in vivo as assessed by the presence of human lamin A/C integrated in the host mouse muscle fibers. We are currently testing whether they could occupy the satellite cell niche in vivo, expand in the niche, and be re-isolated from host muscle to assess whether human satellite cells have self-renewal properties in mouse, and to what extent the mouse and human niches are compatible.

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Event date： 2014.5

Language：English   Presentation type：Poster presentation  

Venue：Lecce   Country：Italy  

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Event date： 2014.4

Language：English   Presentation type：Poster presentation  

Venue：Paris   Country：France  

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Event date： 2014.2

Language：English   Presentation type：Poster presentation  

Venue：Belle-Eglise   Country：France  

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Event date： 2012.9

Language：English   Presentation type：Poster presentation  

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Event date： 2012.6

Language：English   Presentation type：Poster presentation  

Country：Japan  

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Event date： 2011.12

Language：English   Presentation type：Oral presentation (general)  

Venue：Yokohama   Country：Japan  

[Purpose]
Duchenne muscular dystrophy (DMD) is caused by the mutations of the gene encoding dystrophin. Although various skeletal muscle stem cells or progenitors are used to treat DMD, these cells exhibit poor capacity for the engraftment into regenerating muscle. Exploring muscle stem cells suitable for cell therapy, we examined capability of Pax3-positive embryonic and fetal myogenic progenitors (EMPs and FMPs) at different stages for the engraftment to skeletal muscle of DMD model mice.
[Materials and Methods]
Using a mouse strain with the GFP reporter gene targeted into Pax3, we developed cell-sorting method for isolating EMPs and FMPs.
[Results]
We isolated Pax3-GFP cells from embryos at E10.5 and from those at E16.5. While quantitative PCR showed that isolated Pax3-GFP cells at embryonic stage E10.5 (EMPs) contained neural crest cells, Pax3-GFP cells at fetal stage E16.5 (FMPs) had few neural crest cells. When plated on dishes after sorting GFP positive cells, the FMPs activated the myogenic program as demonstrated by sequential expression of myogenic regulatory factors, while the EMPs failed to grow under the same condition. Intramuscular transplantation of FMPs into dystrophic mice resulted in efficient engraftment of adult myofibers with restoration of dystrophin without formation of tumors, whereas mice that received EMPs presented no dystrophin positive myofibers.
[Conclusion]
The data here demonstrate that Pax3(+) FMPs have a high therapeuitc potential in muscular dystrophy. Understanding the cellular and molecular mechanisms underlying efficient transplantation of these MPs would help development of cell therapies for skeletal muscle degeneration diseases.

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Event date： 2011.11

Language：English   Presentation type：Poster presentation  

Venue：Kobe   Country：Japan  

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Event date： 2011.9

Language：English   Presentation type：Poster presentation  

Venue：Awaji   Country：Japan  

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Event date： 2010.11

Language：English   Presentation type：Oral presentation (general)  

Venue：Awaji   Country：Japan  

Purpose/Background:
Duchenne and other types of muscular dystrophies are caused by the loss or mutations of the genes encoding the dystrophin protein complex. These muscle disorders still need effective treatments, and induced pluripotent stem (iPS) cells may constitute an attractive cell therapy because they are pluripotent and can be generated from adult tissues. Little progress has been made toward the use of iPS cells to isolate skeletal muscle progenitors. The goal of this work is the establishment of an effective method to generate myogenic progenitors from mouse iPS cells that can be applicable in the amelioration of muscular dystrophy in future.
Methods/Approaches:
In embryogenesis, all skeletal muscles except for those of the head are derived from the somite. The somite forms the dermomyotome, which gives rise to muscle. Cells expressing the transcription factor Pax3 in the dermomyotome migrate to form myotome. I have used a Pax3GFP/+ mice line to directly isolate Pax3-GFP-expressing dermomyotome cells by flow cytometry from embryos as platelet-derived growth factor receptor-α (PDGFR-α) positive cells. And I generated iPS cells from Pax3GFP/+ mice with Oct3/4, Klf-4 and Sox2.
Results/Perspectives:
Immunohistochemistry of Pax3GFP/+ embryos indicate that dermomyotome was positive for (Pax3)GFP and PDGFR-α. I sorted (Pax3)GFP+PDGFR-α+ cells from Pax3GFP/+ mice embryos. These cells were also positive for the dermomyotome markers En1 and Sim1, the myogenic markers Myf5 and Myogenin by RT-PCR.
Pax3GFP/+ mice-derived iPS cells gave rise to teratoma containing tissues that partially expressed (Pax3)GFP. This iPS clone was differentiated as embryoid bodies. After 12 days induction, (Pax3)GFP+PDGFR-α+ cells was observed by FACS analysis.
The in vivo muscle regeneration potential of these double positive cells will be evaluated by transplanting these cells into DMD mice which is the model mice of Duchenne types of muscular dystrophies.

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Event date： 2009.11

Language：English   Presentation type：Poster presentation  

Venue：Awaji   Country：Japan  

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Event date： 2009.1 - 2009.2

Language：English   Presentation type：Poster presentation  

Venue：Kyoto   Country：Japan  

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