Disease relevance of Myoblasts, Skeletal

• Incubation of L6 skeletal myoblasts for 16 h with cholera toxin but not with pertussis toxin, led to the inhibition of inositol phosphate generation induced by subsequent exposure to vasopressin [1].
• A monoclonal antibody, H-145, the antigen of which is a glycoprotein with a molecular weight of 116 kDa, inhibits the fusion of quail skeletal myoblasts transformed with the temperature-sensitive mutant of Rous sarcoma virus (ts-RSV) (QM-RSV cells) [2].
• Cell transplantation for the treatment of acute myocardial infarction using vascular endothelial growth factor-expressing skeletal myoblasts [3].
• NG2 is associated with multipotential glial precursor cells (O2A progenitor cells), chondroblasts of the developing cartilage, brain capillary endothelial cells, aortic smooth muscle cells, skeletal myoblasts and human melanoma cells [4].

High impact information on Myoblasts, Skeletal

• These observations suggest that either Myf-5 or MyoD is required for the determination of skeletal myoblasts, their propagation, or both during embryonic development and indicate that these factors play, at least in part, functionally redundant roles in myogenesis [5].
• We have assessed the ability of skeletal myoblasts to form long-term, differentiated grafts in ventricular myocardium [6].
• Differentiation of skeletal myoblasts into multinucleated myotubes is a multistep process orchestrated by several families of transcription factors, including myogenic bHLH and NFAT proteins [7].
• Attempts to repair muscle damage in Duchenne muscular dystrophy (DMD) by transplanting skeletal myoblasts directly into muscles are faced with the problem of the limited migration of these cells in the muscles [8].
• Gene trapping in differentiating cell lines: regulation of the lysosomal protease cathepsin B in skeletal myoblast growth and fusion [9].

Biological context of Myoblasts, Skeletal

• Opposing early and late effects of insulin-like growth factor I on differentiation and the cell cycle regulatory retinoblastoma protein in skeletal myoblasts [10].
• Activation of the Raf kinase signal transduction pathway in skeletal myoblasts causes a complete cessation of myofiber formation and muscle gene expression [11].
• In E63 skeletal myoblasts, the treatment of PP2A inhibitors such as okadaic acid and endothall induces an increase of phosphorylation of integrin beta1A and thereby inhibits integrin-induced elevation of cytosolic calcium level and formation of focal adhesions [12].
• MyoD distal regulatory region contains an SRF binding CArG element required for MyoD expression in skeletal myoblasts and during muscle regeneration [13].
• These data collectively indicate that TGF-beta2 restrained differentiation of adult human skeletal myoblasts during propagation without causing irreversible loss of the myoblast phenotype, demonstrating the potential utility of using TGF-beta2 during cultivation and expansion of HuSkMC intended for therapeutic implantation [14].

Anatomical context of Myoblasts, Skeletal

• Rem is expressed in primary skeletal myoblasts and, when overexpressed in C2C12 myoblasts, wild-type Rem inhibits L type Ca2+ channel activity [15].
• Rat skeletal myoblasts and arterial smooth muscle cells express the gene for the A chain but not the gene for the B chain (c-sis) of platelet-derived growth factor (PDGF) and produce a PDGF-like protein [16].
• Co-transfection with hnRNP G represses incorporation in cardiac myoblasts, whereas hTra2beta increases it in skeletal myoblasts [17].
• The Rho family of small GTPases regulates numerous signaling pathways that control the organization of the cytoskeleton, transcription factor activity, and many aspects of the differentiation of skeletal myoblasts [18].
• Fusion of chick embryo skeletal myoblasts: interactions of prostaglandin E1, adenosine 3':5' monophosphate, and calcium influx [19].

Associations of Myoblasts, Skeletal with chemical compounds

• To study the role of (pro)collagen synthesis in the differentiation of rat L6 skeletal myoblasts, a specific inhibitor of collagen synthesis, ethyl-3,4-dihydroxybenzoate (DHB), was utilized [20].
• We investigated the effect of trifluoperazine (TFP), a calmodulin antagonist, on the fusion of chick skeletal myoblasts in culture [21].
• Possible involvement of a cell surface glycoprotein in the differentiation of skeletal myoblasts [22].
• Regulation of protein kinase C by cyclic adenosine 3':5'-monophosphate and a tumor promoter in skeletal myoblasts [23].
• These results support a modulatory effect of insulin on the BK signaling system via a tyrosine kinase in L8 rat skeletal myoblasts that results in increased IP3 formation [24].

Gene context of Myoblasts, Skeletal

• The oncogenic forms of N-ras or H-ras prevent skeletal myoblast differentiation [25].
• Expression of the dominant negative protein in C2C12 skeletal myoblasts blocked the differentiation-induced expression of the SRF target genes skeletal alpha-actin and alpha-myosin heavy chain and blocked differentiation of the myoblasts to myotubes in vitro [26].
• Regulation of Notch1 activity is critical for cell fate decisions and differentiation of skeletal myoblasts [27].
• Here, we investigated the direct effect of CNTF on skeletal myoblasts of adult human [28].
• Cell-type specific adhesive interactions of skeletal myoblasts with thrombospondin-1 [29].

Analytical, diagnostic and therapeutic context of Myoblasts, Skeletal

• Transplantation of skeletal myoblasts secreting an IL-1 inhibitor modulates adverse remodeling in infarcted murine myocardium [30].
• Reverse transcriptase-polymerase chain reaction analysis of alpha 7 mRNA indicated that the X1 and X2 isoforms were present in equal amounts in mouse skeletal myoblasts and adult heart [31].
• Primary neonatal rat and mouse skeletal myoblast cultures were shown to express PAR-2 in polymerase chain reaction and immunocytochemical studies [32].
• Immunofluorescence microscopy has been used to demonstrate that X22, a monoclonal antibody specific for clathrin heavy chain, localizes in repetitive bands that appear soon after the fusion of skeletal myoblasts into multinucleate fibers [33].
• METHODS: To analyze intracellular pathways leading to iNOS induction, rat skeletal myoblasts were incubated with inflammatory cytokines and assessed for iNOS expression by Western blot and Griess reaction [34].

References