Limits...
Skeletal muscle stem cells.

Chen JC, Goldhamer DJ - Reprod. Biol. Endocrinol. (2003)

Bottom Line: Satellite cells are myogenic stem cells responsible for the post-natal growth, repair and maintenance of skeletal muscle.Recent advances have altered the long-standing view of the satellite cell as a committed myogenic stem cell derived directly from the fetal myoblast.The experimental basis for this evolving perspective will be highlighted as will the relationship between the satellite cell and other newly discovered muscle stem cell populations.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Molecular and Cell Biology, Center for Regenerative Biology, University of Connecticut, 1392 Storrs Road Unit 4243, Storrs, CT 06269-4243, USA. jennifer.chen@uconn.edu

ABSTRACT
Satellite cells are myogenic stem cells responsible for the post-natal growth, repair and maintenance of skeletal muscle. This review focuses on the basic biology of the satellite cell with emphasis on its role in muscle repair and parallels between embryonic myogenesis and muscle regeneration. Recent advances have altered the long-standing view of the satellite cell as a committed myogenic stem cell derived directly from the fetal myoblast. The experimental basis for this evolving perspective will be highlighted as will the relationship between the satellite cell and other newly discovered muscle stem cell populations. Finally, advances and prospects for cell-based therapies for muscular dystrophies will be addressed.

Show MeSH

Related in: MedlinePlus

Model for the development, activation, and maintenance of the satellite cell. Upon skeletal muscle injury, quiescent satellite cells expressing Pax-7 and Foxk1 are activated to proliferate, up-regulating the myogenic determination factors, MyoD and Myf-5 [13-17], the myoblast marker desmin [16,79], and Wnts 5a and 5b [12]. Satellite cell activation is regulated by the Notch signaling pathway [25], and proliferation is stimulated by a number of growth factors, including basic FGF, insulin-like growth factor-1, and HGF/SF [26,32,80]. Transition from proliferation to differentiation, which is accompanied by the down-regulation of Pax-7 [57] and up-regulation of Myogenin and MRF-4 [13,14,16], is dependent on both MyoD [36] and the Foxk1 pathway [33,34]. Candidate satellite cell progenitors, which must activate Pax-7 for satellite cell development [57], include embryonic myoblast precursors, fetal myoblasts, and vessel-associated mesoangioblasts, the latter of which exhibits strong myogenic potential [60-62]. Additionally, bone marrow-derived (BMD) stem cells can contribute directly to quiescent satellite cells and regenerating muscle fibers following injury [54,65,68], and muscle SP cells have been used with some success in myoblast transplantation experiments into dystrophic muscle [53,54]. Importantly, members of the Wnt family of secreted glycoproteins can convert SP cells favoring the hematopoietic fate into highly myogenic cells [12].
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC305326&req=5

Figure 1: Model for the development, activation, and maintenance of the satellite cell. Upon skeletal muscle injury, quiescent satellite cells expressing Pax-7 and Foxk1 are activated to proliferate, up-regulating the myogenic determination factors, MyoD and Myf-5 [13-17], the myoblast marker desmin [16,79], and Wnts 5a and 5b [12]. Satellite cell activation is regulated by the Notch signaling pathway [25], and proliferation is stimulated by a number of growth factors, including basic FGF, insulin-like growth factor-1, and HGF/SF [26,32,80]. Transition from proliferation to differentiation, which is accompanied by the down-regulation of Pax-7 [57] and up-regulation of Myogenin and MRF-4 [13,14,16], is dependent on both MyoD [36] and the Foxk1 pathway [33,34]. Candidate satellite cell progenitors, which must activate Pax-7 for satellite cell development [57], include embryonic myoblast precursors, fetal myoblasts, and vessel-associated mesoangioblasts, the latter of which exhibits strong myogenic potential [60-62]. Additionally, bone marrow-derived (BMD) stem cells can contribute directly to quiescent satellite cells and regenerating muscle fibers following injury [54,65,68], and muscle SP cells have been used with some success in myoblast transplantation experiments into dystrophic muscle [53,54]. Importantly, members of the Wnt family of secreted glycoproteins can convert SP cells favoring the hematopoietic fate into highly myogenic cells [12].

Mentions: Several signals and growth factors have been implicated in promotion of satellite cell activation and proliferation (Figure 1). For example, the Notch signaling pathway, which is activated upon muscle injury, regulates satellite cell transition from quiescence to proliferation in single fiber cultures, thereby expanding the myoblast population in injured muscle [25]. Basic fibroblast growth factor (bFGF) stimulates satellite cell proliferation while inhibiting differentiation [2]. bFGF also promotes muscle regeneration in mdx mice [26], which undergo repeated cycles of degeneration and regeneration resulting from a mutation in the dystrophin gene; in humans, deficiency of dystrophin causes Duchenne muscular dystrophy [27,28]. In addition to expressing all known FGF receptors [29,30], satellite cells also express the tyrosine kinase receptor c-met [16,31]. The c-met ligand, hepatocyte growth factor/scatter factor (HGF/SF), is also a known activator of satellite cells [29,32].


Skeletal muscle stem cells.

Chen JC, Goldhamer DJ - Reprod. Biol. Endocrinol. (2003)

Model for the development, activation, and maintenance of the satellite cell. Upon skeletal muscle injury, quiescent satellite cells expressing Pax-7 and Foxk1 are activated to proliferate, up-regulating the myogenic determination factors, MyoD and Myf-5 [13-17], the myoblast marker desmin [16,79], and Wnts 5a and 5b [12]. Satellite cell activation is regulated by the Notch signaling pathway [25], and proliferation is stimulated by a number of growth factors, including basic FGF, insulin-like growth factor-1, and HGF/SF [26,32,80]. Transition from proliferation to differentiation, which is accompanied by the down-regulation of Pax-7 [57] and up-regulation of Myogenin and MRF-4 [13,14,16], is dependent on both MyoD [36] and the Foxk1 pathway [33,34]. Candidate satellite cell progenitors, which must activate Pax-7 for satellite cell development [57], include embryonic myoblast precursors, fetal myoblasts, and vessel-associated mesoangioblasts, the latter of which exhibits strong myogenic potential [60-62]. Additionally, bone marrow-derived (BMD) stem cells can contribute directly to quiescent satellite cells and regenerating muscle fibers following injury [54,65,68], and muscle SP cells have been used with some success in myoblast transplantation experiments into dystrophic muscle [53,54]. Importantly, members of the Wnt family of secreted glycoproteins can convert SP cells favoring the hematopoietic fate into highly myogenic cells [12].
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC305326&req=5

Figure 1: Model for the development, activation, and maintenance of the satellite cell. Upon skeletal muscle injury, quiescent satellite cells expressing Pax-7 and Foxk1 are activated to proliferate, up-regulating the myogenic determination factors, MyoD and Myf-5 [13-17], the myoblast marker desmin [16,79], and Wnts 5a and 5b [12]. Satellite cell activation is regulated by the Notch signaling pathway [25], and proliferation is stimulated by a number of growth factors, including basic FGF, insulin-like growth factor-1, and HGF/SF [26,32,80]. Transition from proliferation to differentiation, which is accompanied by the down-regulation of Pax-7 [57] and up-regulation of Myogenin and MRF-4 [13,14,16], is dependent on both MyoD [36] and the Foxk1 pathway [33,34]. Candidate satellite cell progenitors, which must activate Pax-7 for satellite cell development [57], include embryonic myoblast precursors, fetal myoblasts, and vessel-associated mesoangioblasts, the latter of which exhibits strong myogenic potential [60-62]. Additionally, bone marrow-derived (BMD) stem cells can contribute directly to quiescent satellite cells and regenerating muscle fibers following injury [54,65,68], and muscle SP cells have been used with some success in myoblast transplantation experiments into dystrophic muscle [53,54]. Importantly, members of the Wnt family of secreted glycoproteins can convert SP cells favoring the hematopoietic fate into highly myogenic cells [12].
Mentions: Several signals and growth factors have been implicated in promotion of satellite cell activation and proliferation (Figure 1). For example, the Notch signaling pathway, which is activated upon muscle injury, regulates satellite cell transition from quiescence to proliferation in single fiber cultures, thereby expanding the myoblast population in injured muscle [25]. Basic fibroblast growth factor (bFGF) stimulates satellite cell proliferation while inhibiting differentiation [2]. bFGF also promotes muscle regeneration in mdx mice [26], which undergo repeated cycles of degeneration and regeneration resulting from a mutation in the dystrophin gene; in humans, deficiency of dystrophin causes Duchenne muscular dystrophy [27,28]. In addition to expressing all known FGF receptors [29,30], satellite cells also express the tyrosine kinase receptor c-met [16,31]. The c-met ligand, hepatocyte growth factor/scatter factor (HGF/SF), is also a known activator of satellite cells [29,32].

Bottom Line: Satellite cells are myogenic stem cells responsible for the post-natal growth, repair and maintenance of skeletal muscle.Recent advances have altered the long-standing view of the satellite cell as a committed myogenic stem cell derived directly from the fetal myoblast.The experimental basis for this evolving perspective will be highlighted as will the relationship between the satellite cell and other newly discovered muscle stem cell populations.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Molecular and Cell Biology, Center for Regenerative Biology, University of Connecticut, 1392 Storrs Road Unit 4243, Storrs, CT 06269-4243, USA. jennifer.chen@uconn.edu

ABSTRACT
Satellite cells are myogenic stem cells responsible for the post-natal growth, repair and maintenance of skeletal muscle. This review focuses on the basic biology of the satellite cell with emphasis on its role in muscle repair and parallels between embryonic myogenesis and muscle regeneration. Recent advances have altered the long-standing view of the satellite cell as a committed myogenic stem cell derived directly from the fetal myoblast. The experimental basis for this evolving perspective will be highlighted as will the relationship between the satellite cell and other newly discovered muscle stem cell populations. Finally, advances and prospects for cell-based therapies for muscular dystrophies will be addressed.

Show MeSH
Related in: MedlinePlus