Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of {alpha}7 integrin-expressing myoblasts

Epting, Conrad L; Lopez, Javier E; Pedersen, Anissa; Brown, Courtney; Spitz, Paul; Ursell, Philip C; Bernstein, Harold S

doi:10.1016/j.yexcr.2007.11.010

Title: Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of {alpha}7 integrin-expressing myoblasts

Full Record
Other Related Research

Abstract

Skeletal muscle repair occurs through a programmed series of events including myogenic precursor activation, myoblast proliferation, and differentiation into new myofibers. We previously identified a role for Stem cell antigen-1 (Sca-1) in myoblast proliferation and differentiation in vitro. We demonstrated that blocking Sca-1 expression resulted in sustained myoblast cell division. Others have since demonstrated that Sca-1-null myoblasts display a similar phenotype when cultured ex vivo. To test the importance of Sca-1 during myogenesis in vivo, we employed a myonecrotic injury model in Sca-1{sup -/-} and Sca-1{sup +/+} mice. Our results demonstrate that Sca-1{sup -/-} myoblasts exhibit a hyperproliferative response consisting of prolonged and accelerated cell division in response to injury. This leads to delayed myogenic differentiation and muscle repair. These data provide the first in vivo evidence for Sca-1 as a regulator of myoblast proliferation during muscle regeneration. These studies also suggest that the balance between myogenic precursor proliferation and differentiation is critical to normal muscle repair.

Authors:

Epting, Conrad L ^[1]; Lopez, Javier E ^[1]; Pedersen, Anissa ^[1]; Brown, Courtney ^[1]; Spitz, Paul ^[1]; Ursell, Philip C ^[2]; Bernstein, Harold S ^[1]

Cardiovascular Research Institute, University of California, San Francisco (United States)
Department of Pathology, University of California, San Francisco (United States)

Publication Date:: Mon Mar 10 00:00:00 EDT 2008

OSTI Identifier:: 21045951

Resource Type:: Journal Article

Journal Name:: Experimental Cell Research

Additional Journal Information:: Journal Volume: 314; Journal Issue: 5; Other Information: DOI: 10.1016/j.yexcr.2007.11.010; PII: S0014-4827(07)00524-1; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0014-4827

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; ANTIGENS; BIOLOGICAL REPAIR; CELL DIVISION; IN VITRO; IN VIVO; INJURIES; MICE; MYOBLASTS; PHENOTYPE; STEM CELLS

Citation Formats


                    Epting, Conrad L, Department of Pediatrics, University of California, San Francisco, Lopez, Javier E, Department of Medicine, University of California, San Francisco, Pedersen, Anissa, Brown, Courtney, Department of Medicine, University of California, San Francisco, Spitz, Paul, Ursell, Philip C, Bernstein, Harold S, Department of Pediatrics, University of California, San Francisco, Department of Medicine, University of California, San Francisco, and Institute for Regeneration Medicine, University of California, San Francisco. Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of {alpha}7 integrin-expressing myoblasts.  United States: N. p., 2008. 
        Web.  doi:10.1016/j.yexcr.2007.11.010.

Copy to clipboard


                    Epting, Conrad L, Department of Pediatrics, University of California, San Francisco, Lopez, Javier E, Department of Medicine, University of California, San Francisco, Pedersen, Anissa, Brown, Courtney, Department of Medicine, University of California, San Francisco, Spitz, Paul, Ursell, Philip C, Bernstein, Harold S, Department of Pediatrics, University of California, San Francisco, Department of Medicine, University of California, San Francisco, & Institute for Regeneration Medicine, University of California, San Francisco. Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of {alpha}7 integrin-expressing myoblasts.  United States.  https://doi.org/10.1016/j.yexcr.2007.11.010

Copy to clipboard


                    Epting, Conrad L, Department of Pediatrics, University of California, San Francisco, Lopez, Javier E, Department of Medicine, University of California, San Francisco, Pedersen, Anissa, Brown, Courtney, Department of Medicine, University of California, San Francisco, Spitz, Paul, Ursell, Philip C, Bernstein, Harold S, Department of Pediatrics, University of California, San Francisco, Department of Medicine, University of California, San Francisco, and Institute for Regeneration Medicine, University of California, San Francisco. 2008.  
        "Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of {alpha}7 integrin-expressing myoblasts".  United States.  https://doi.org/10.1016/j.yexcr.2007.11.010.

Copy to clipboard


                    
@article{osti_21045951,

  title        = {Stem cell antigen-1 regulates the tempo of muscle repair through effects on proliferation of {alpha}7 integrin-expressing myoblasts},

  author       = {Epting, Conrad L and Department of Pediatrics, University of California, San Francisco and Lopez, Javier E and Department of Medicine, University of California, San Francisco and Pedersen, Anissa and Brown, Courtney and Department of Medicine, University of California, San Francisco and Spitz, Paul and Ursell, Philip C and Bernstein, Harold S and Department of Pediatrics, University of California, San Francisco and Department of Medicine, University of California, San Francisco and Institute for Regeneration Medicine, University of California, San Francisco},

  abstractNote = {Skeletal muscle repair occurs through a programmed series of events including myogenic precursor activation, myoblast proliferation, and differentiation into new myofibers. We previously identified a role for Stem cell antigen-1 (Sca-1) in myoblast proliferation and differentiation in vitro. We demonstrated that blocking Sca-1 expression resulted in sustained myoblast cell division. Others have since demonstrated that Sca-1-null myoblasts display a similar phenotype when cultured ex vivo. To test the importance of Sca-1 during myogenesis in vivo, we employed a myonecrotic injury model in Sca-1{sup -/-} and Sca-1{sup +/+} mice. Our results demonstrate that Sca-1{sup -/-} myoblasts exhibit a hyperproliferative response consisting of prolonged and accelerated cell division in response to injury. This leads to delayed myogenic differentiation and muscle repair. These data provide the first in vivo evidence for Sca-1 as a regulator of myoblast proliferation during muscle regeneration. These studies also suggest that the balance between myogenic precursor proliferation and differentiation is critical to normal muscle repair.},

  doi          = {10.1016/j.yexcr.2007.11.010},

  url          = {https://www.osti.gov/biblio/21045951},
  journal      = {Experimental Cell Research},

  issn         = {0014-4827},

  number       = 5,

  volume       = 314,

  place        = {United States},

  year         = {Mon Mar 10 00:00:00 EDT 2008},

  month        = {Mon Mar 10 00:00:00 EDT 2008}

}

Copy to clipboard

Journal Article:

https://doi.org/10.1016/j.yexcr.2007.11.010

Other availability

Find in Google Scholar

Search WorldCat to find libraries that may hold this journal

Save / Share:

Export Metadata

Save to My Library

Similar records in OSTI.GOV collections:

TGF-{beta}'s delay skeletal muscle progenitor cell differentiation in an isoform-independent manner

Journal Article Schabort, Elske; Merwe, Mathilde; Loos, Benjamin; ... - Experimental Cell Research

Satellite cells are a quiescent heterogenous population of mononuclear stem and progenitor cells which, once activated, differentiate into myotubes and facilitate skeletal muscle repair or growth. The Transforming Growth Factor-{beta} (TGF-{beta}) superfamily members are elevated post-injury and their importance in the regulation of myogenesis and wound healing has been demonstrated both in vitro and in vivo. Most studies suggest a negative role for TGF-{beta} on satellite cell differentiation. However, none have compared the effect of these three isoforms on myogenesis in vitro. This is despite known isoform-specific effects of TGF-{beta}1, -{beta}2 and -{beta}3 on wound repair in other tissues. Inmore »« less
https://doi.org/10.1016/j.yexcr.2008.10.037
Brain and muscle Arnt-like 1 promotes skeletal muscle regeneration through satellite cell expansion

Journal Article Chatterjee, Somik; Yin, Hongshan; Nam, Deokhwa; ... - Experimental Cell Research

Circadian clock is an evolutionarily conserved timing mechanism governing diverse biological processes and the skeletal muscle possesses intrinsic functional clocks. Interestingly, although the essential clock transcription activator, Brain and muscle Arnt-like 1 (Bmal1), participates in maintenance of muscle mass, little is known regarding its role in muscle growth and repair. In this report, we investigate the in vivo function of Bmal1 in skeletal muscle regeneration using two muscle injury models. Bmal1 is highly up-regulated by cardiotoxin injury, and its genetic ablation significantly impairs regeneration with markedly suppressed new myofiber formation and attenuated myogenic induction. A similarly defective regenerative response ismore »« less
https://doi.org/10.1016/J.YEXCR.2014.08.041
ERK2 is required for efficient terminal differentiation of skeletal myoblasts

Journal Article Ju, Li; Johnson, Sally - Biochemical and Biophysical Research Communications

Terminal differentiation of skeletal myoblasts involves alignment of the mononucleated cells, fusion into multinucleated syncitia, and transcription of muscle-specific genes. Myogenesis in vivo is regulated partially by IGF-I initiated signaling that results in activation of an intracellular phosphatidylinositol 3 kinase (PI3K) signaling cascade. Downstream signaling through the Raf/MEK/ERK axis, a pathway initiated by IGF-I, also is implicated in the regulation of muscle formation. The involvement of ERK1 and ERK2 during myogenesis was examined in C2C12 myoblasts. C2C12 myoblasts stably expressing a small interfering RNA (siRNA) directed against ERK1 or ERK2 were created. Both of the kinases were reduced to tracemore »« less
Inhibition of Rev-erbα ameliorates muscular dystrophy

Journal Article Xiong, Xuekai; Gao, Hongbo; Lin, Yayu; ... - Experimental Cell Research

Highlights: • Rev-erbα ablation in mdx mice protects against muscle damage and wasting. • Loss of Rev-erbα promoted regenerative myogenesis in mdx mice. • Rev-erbα deficiency in dystrophic muscle reduced inflammatory response. • Loss of Rev-erbα in mdx primary myoblasts promoted proliferation and differentiation. Duchene muscular dystrophy leads to progressive muscle structural and functional decline due to chronic degenerative-regenerative cycles. Enhancing the regenerative capacity of dystrophic muscle provides potential therapeutic options. We previously demonstrated that the circadian clock repressor Rev-erbα inhibited myogenesis and Rev-erbα ablation enhanced muscle regeneration. Here we show that Rev-erbα deficiency in the dystrophin-deficient mdx mice promotesmore »« less
https://doi.org/10.1016/J.YEXCR.2021.112766
AP-2{alpha} suppresses skeletal myoblast proliferation and represses fibroblast growth factor receptor 1 promoter activity

Journal Article Mitchell, Darrion - Experimental Cell Research

Skeletal muscle development is partly characterized by myoblast proliferation and subsequent differentiation into postmitotic muscle fibers. Developmental regulation of expression of the fibroblast growth factor receptor 1 (FGFR1) gene is required for normal myoblast proliferation and muscle formation. As a result, FGFR1 promoter activity is controlled by multiple transcriptional regulatory proteins during both proliferation and differentiation of myogenic cells. The transcription factor AP-2{alpha} is present in nuclei of skeletal muscle cells and suppresses myoblast proliferation in vitro. Since FGFR1 gene expression is tightly linked to myoblast proliferation versus differentiation, the FGFR1 promoter was examined for candidate AP-2{alpha} binding sites. Mutagenesismore »« less
https://doi.org/10.1016/J.YEXCR.2009.08.008

Similar Records