The transcription of MyoD1 and myogenin genes in thymic cells in vivo

Grounds, Miranda D.; Garrett, Kerryn L.; Beilharz, Manfred W.

doi:10.1016/0014-4827(92)90391-k

Cited by 42 publications

(27 citation statements)

References 29 publications

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“…1A). A typical niche of G8 pos cells (shown at higher magnification in factor MyoD (12,(17)(18)(19), a property that gives cells myogenic potential (21,22), we double-labeled epithelial explants with fluorescein-tagged G8 mAb and DNA dendrimers conjugated with both an antisense oligonucleotide sequence for MyoD mRNA and the fluorochrome Cy3 (23,24). The results showed that the G8 pos cells associated with the lens epithelium also expressed MyoD mRNA (Fig.…”

Section: Resultsmentioning

confidence: 93%

“…In vivo, these cells are incorporated into somites where they function instead as cellsignaling centers that promote the myogenic differentiation of surrounding skeletal muscle progenitor cells through their release of Noggin, a bone morphogenetic protein inhibitor (16). G8 pos / MyoD pos cells also are incorporated into tissues that lack skeletal muscle (12,(17)(18)(19), including the embryonic lens (20), where our studies now suggest they play a principal role in wound repair and are a source of disease-causing myofibroblasts.…”

mentioning

confidence: 87%

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Unique precursors for the mesenchymal cells involved in injury response and fibrosis

Walker

Zhai

Zhang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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We investigated an alternative pathway for emergence of the mesenchymal cells involved in epithelial sheet wound healing and a source of myofibroblasts that cause fibrosis. Using a mock cataract surgery model, we discovered a unique subpopulation of polyploid mesenchymal progenitors nestled in small niches among lens epithelial cells that expressed the surface antigen G8 and mRNA for the myogenic transcription factor MyoD. These cells rapidly responded to wounding of the lens epithelium with population expansion, acquisition of a mesenchymal phenotype, and migration to the wound edges where they regulate the wound response of the epithelium. These mesenchymal cells also were a principal source of myofibroblasts that emerged following lens injury and were responsible for fibrotic disease of the lens that occurs following cataract surgery. These studies provide insight into the mechanisms of wound-healing and fibrosis.lens | myofibroblast | wound healing | migration | posterior capsule opacification

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Section: Resultsmentioning

confidence: 93%

mentioning

confidence: 87%

Unique precursors for the mesenchymal cells involved in injury response and fibrosis

Walker

Zhai

Zhang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Quiescent satellite cells express the paired box transcription factor family member Pax7 (Seale et al, 2000). When activated, they coexpress Pax7 with MyoD (Grounds et al, 1992;Yablonka-Reuveni and Rivera, 1994;Zammit et al, 2002), a key transcription factor for myogenic differentiation and a member of the myogenic regulatory factor (MRFs) family, comprising MyoD, Myf5, myogenin and Mrf4 (reviewed by Tajbakhsh and Buckingham, 2000 (Zammit et al, 2004;Nagata et al, 2006). A similar mechanism has also been described during muscle growth in chicken (Halevy et al, 2004).…”

Section: Introductionmentioning

confidence: 91%

Pax7 and myogenic progression in skeletal muscle satellite cells

Zammit

Relaix

Nagata

et al. 2006

Journal of Cell Science

502

431

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Skeletal muscle growth and regeneration are attributed to satellite cells - muscle stem cells resident beneath the basal lamina that surrounds each myofibre. Quiescent satellite cells express the transcription factor Pax7 and when activated, coexpress Pax7 with MyoD. Most then proliferate, downregulate Pax7 and differentiate. By contrast, others maintain Pax7 but lose MyoD and return to a state resembling quiescence. Here we show that Pax7 is able to drive transcription in quiescent and activated satellite cells, and continues to do so in those cells that subsequently cease proliferation and withdraw from immediate differentiation. We found that constitutive expression of Pax7 in satellite-cell-derived myoblasts did not affect MyoD expression or proliferation. Although maintained expression of Pax7 delayed the onset of myogenin expression it did not prevent, and was compatible with, myogenic differentiation. Constitutive Pax7 expression in a Pax7-null C2C12 subclone increased the proportion of cells expressing MyoD, showing that Pax7 can act genetically upstream of MyoD. However these Pax7-null cells were unable to differentiate into normal myotubes in the presence of Pax7. Therefore Pax7 may be involved in maintaining proliferation and preventing precocious differentiation, but does not promote quiescence.

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“…Grounds et al (Grounds et al, 1992) demonstrated that Myod1 and myogenin (Myog) gene expression can be used as markers for the very early detection of migrating myoblasts during muscle regeneration. Hence, we determined the expression of Myod1 and Myog in the regenerating tissue.…”

Section: Early Expression Of Myogenic Genes In Regenerating Mstn -/-Mmentioning

confidence: 99%

Improved muscle healing through enhanced regeneration and reduced fibrosis in myostatin-null mice

McCroskery

Thomas

Platt

et al. 2005

Journal of Cell Science

180

140

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Numerous stimulatory growth factors that can influence muscle regeneration are known. Recently, it has been demonstrated that neutralization of muscle growth inhibitory factors, such as myostatin (Mstn; also known as growth differentiation factor 8, Gdf8), also leads to increased muscle regeneration in mdx mice that are known to have cycles of degeneration. However, the precise mechanism by which Mstn regulates muscle regeneration has not yet been fully determined. To investigate the role of Mstn in adult skeletal muscle regeneration, wild-type and myostatin-null (Mstn-/-) mice were injured with notexin. Forty-eight hours after injury, accelerated migration and enhanced accretion of myogenic cells (MyoD1+) and macrophages (Mac-1+) was observed at the site of regeneration in Mstn-/- muscle as compared with wild-type muscle. Inflammatory cell numbers decreased more rapidly in the Mstn-/- muscle, indicating that the whole process of inflammatory cell response is accelerated in Mstn-/- mice. Consistent with this result, the addition of recombinant Mstn reduced the activation of satellite cells (SCs) and chemotactic movements of both myoblasts and macrophages ex vivo. Examination of regenerated muscle (28 days after injury) also revealed that Mstn-/- mice showed increased expression of decorin mRNA, reduced fibrosis and improved healing as compared with wild-type mice. On the basis of these results, we propose that Mstn negatively regulates muscle regeneration not only by controlling SC activation but also by regulating the migration of myoblasts and macrophages to the site of injury. Thus, antagonists of Mstn could potentially be useful as pharmacological agents for the treatment of disorders of overt degeneration and regeneration.

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The transcription of MyoD1 and myogenin genes in thymic cells in vivo

Cited by 42 publications

References 29 publications

Unique precursors for the mesenchymal cells involved in injury response and fibrosis

Unique precursors for the mesenchymal cells involved in injury response and fibrosis

Pax7 and myogenic progression in skeletal muscle satellite cells

Improved muscle healing through enhanced regeneration and reduced fibrosis in myostatin-null mice

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