NeuroM and MyoD are expressed in separate subpopulations of cells in the pregastrulating epiblast

Strony, Robert; Gerhart, Jacquelyn; Tornambe, Dolores; Perlman, Jordanna; Neely, Christine; Dare, Jeffrey; Stewart, Benjamin; George‐Weinstein, Mindy

doi:10.1016/j.modgep.2004.09.006

Cited by 19 publications

(50 citation statements)

References 32 publications

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“…Double labeling was also performed with the G8 mAb and goat polyclonal antibodies to Noggin (AF719; R&D Systems, Minneapolis, MN, USA) and rabbit polyclonal antibodies to filensin [42] and CP49 [43], [44]. Controls for non-specific staining included the E12 IgM mAb [29], 2H3 IgG mAb to neurofilament protein [45] and a goat polyclonal antiserum to the homeobox protein LBX1 expressed in the central nervous system and some developing muscles [46] (Santa Cruz Biotechnology, Dallas, TX, USA). Monoclonal antibodies to vimentin, sarcomeric myosins, the 12101 antigen, troponin T and neurofilament protein were obtained from the Developmental Studies Hybridoma Bank (developed under the auspices of the NICHD and maintained by the University of Iowa, Dept.…”

Section: Methodsmentioning

confidence: 99%

“…The propensity of Myo/Nog cells to respond to wounding reflects, in part, their innate capacity for migration and expression of muscle proteins [20]–[22], [24], [25], [29]. When removed from embryonic and fetal tissues and cultured in serum-free medium, they translate MyoD mRNA and undergo terminal skeletal muscle differentiation [24], [25], [28], [29]. In vivo , Myo/Nog cells do not appear to translate MyoD mRNA or synthesize sarcomeric proteins under homeostatic conditions [21], [25], [30].…”

Section: Introductionmentioning

confidence: 99%

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Myo/Nog Cells: Targets for Preventing the Accumulation of Skeletal Muscle-Like Cells in the Human Lens

et al. 2014

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Posterior capsule opacification (PCO) is a vision impairing condition that arises in some patients following cataract surgery. The fibrotic form of PCO is caused by myofibroblasts that may emerge in the lens years after surgery. In the chick embryo lens, myofibroblasts are derived from Myo/Nog cells that are identified by their expression of the skeletal muscle specific transcription factor MyoD, the bone morphogenetic protein inhibitor Noggin, and the epitope recognized by the G8 monoclonal antibody. The goal of this study was to test the hypothesis that depletion of Myo/Nog cells will prevent the accumulation of myofibroblasts in human lens tissue. Myo/Nog cells were present in anterior, equatorial and bow regions of the human lens, cornea and ciliary processes. In anterior lens tissue removed by capsulorhexis, Myo/Nog cells had synthesized myofibroblast and skeletal muscle proteins, including vimentin, MyoD and sarcomeric myosin. Alpha smooth muscle actin (α-SMA) was detected in a subpopulation of Myo/Nog cells. Areas of the capsule denuded of epithelial cells were surrounded by Myo/Nog cells. Some of these cell free areas contained a wrinkle in the capsule. Depletion of Myo/Nog cells eliminated cells expressing skeletal muscle proteins in 5-day cultures but did not affect cells immunoreactive for beaded filament proteins that accumulate in differentiating lens epithelial cells. Transforming growth factor-betas 1 and 2 that mediate an epithelial-mesenchymal transition, did not induce the expression of skeletal muscle proteins in lens cells following Myo/Nog cell depletion. This study demonstrates that Myo/Nog cells in anterior lens tissue removed from cataract patients have undergone a partial differentiation to skeletal muscle. Myo/Nog cells appear to be the source of skeletal muscle-like cells in explants of human lens tissue. Targeting Myo/Nog cells with the G8 antibody during cataract surgery may reduce the incidence of PCO.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Myo/Nog Cells: Targets for Preventing the Accumulation of Skeletal Muscle-Like Cells in the Human Lens

et al. 2014

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“…The cell type we investigated as a candidate for the mesenchymal precursor cell in our lens injury model is identified by its expression of the cell-surface antigen G8 and messenger RNA (mRNA) for the skeletal muscle-specific transcription factor MyoD, but not MyoD protein. Cells with these properties were originally identified as a subpopulation of the epiblast (12)(13)(14), a tissue that gives rise to all three germ layers of the embryo (15). G8 and MyoD mRNA expressing epiblast cells are capable of undergoing myogenesis when removed from the embryo and placed in culture (12)(13)(14).…”

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confidence: 99%

“…Cells with these properties were originally identified as a subpopulation of the epiblast (12)(13)(14), a tissue that gives rise to all three germ layers of the embryo (15). G8 and MyoD mRNA expressing epiblast cells are capable of undergoing myogenesis when removed from the embryo and placed in culture (12)(13)(14). 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).…”

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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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“…They were identified by their expression of mRNA for the skeletal muscle specific transcription factor MyoD, the bone morphogenetic protein (BMP) inhibitor Noggin and the cell surface protein recognized by the G8 monoclonal antibody (mAb)[1, 4–7]. During gastrulation, Myo/Nog cells become widely distributed in small numbers throughout the embryo [1, 3, 8].…”

Section: Introductionmentioning

confidence: 99%

Role of Myo/Nog Cells in Neuroprotection: Evidence from the Light Damaged Retina

et al. 2017

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PurposeTo identify Myo/Nog cells in the adult retina and test their role in protecting retinal photoreceptors from light damage.MethodsLight damage was induced by exposing albino rats raised in dim cyclic light to 1000 lux light for 24 hours. In one group of rats, Myo/Nog cells were purified from rat brain tissue by magnetic cell sorting following binding of the G8 monoclonal antibody (mAb). These cells were injected into the vitreous humour of the eye within 2 hours following bright light exposure. Retinal function was assessed using full-field, flash electroretinogram (ERG) before and after treatment. The numbers of Myo/Nog cells, apoptotic photoreceptors, and the expression of glial fibrillary acidic protein (GFAP) in Muller cells were assessed by immunohistochemistry.ResultsMyo/Nog cells were present in the undamaged retina in low numbers. Light induced damage increased their numbers, particularly in the choroid, ganglion cell layer and outer plexiform layer. Intravitreal injection of G8-positive (G8+) cells harvested from brain mitigated all the effects of light damage examined, i.e. loss of retinal function (ERG), death of photoreceptors and the stress-induced expression of GFAP in Muller cells. Some of the transplanted G8+ cells were integrated into the retina from the vitreous.ConclusionsMyo/Nog cells are a subpopulation of cells that are present in the adult retina. They increase in number in response to light induced stress. Intravitreal injection of Myo/Nog cells was protective to the retina, in part, by reducing retinal stress as measured by the Muller cell response. These results suggest that Myo/Nog cells, or the factors they produce, are neuroprotective and may be therapeutic in neurodegenerative retinal diseases.

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NeuroM and MyoD are expressed in separate subpopulations of cells in the pregastrulating epiblast

Cited by 19 publications

References 32 publications

Myo/Nog Cells: Targets for Preventing the Accumulation of Skeletal Muscle-Like Cells in the Human Lens

Myo/Nog Cells: Targets for Preventing the Accumulation of Skeletal Muscle-Like Cells in the Human Lens

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

Role of Myo/Nog Cells in Neuroprotection: Evidence from the Light Damaged Retina

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