Vimentin and Desmin
Masahiko Mori in Histochemistry of the Salivary Glands, 2019
Vimentin and desmin are intermediate sized filaments in cells of nonepithelial origin. Immunohistochemical demonstrations of vimentin and desmin have been shown in rodent salivary glands. Salivary glands in the rat and mouse showed very slight staining with polyclonal antiserum of vimentin and desmin in striated and excretory ducts, as well as in granular convoluted tubule cells. Salivary glands in man stained differently with polyclonal vimentin and desmin, and monoclonal antibodies. Monoclonal antibodies of vimentin and desmin failed to stain salivary gland tissue either acinar or ductal cells. Epithelial tumor cells of salivary pleomorphic adenomas stained variably for keratin proteins, as well as for vimentin, which seems to be characteristic for mesenchymal cells. Desmin is a well-known marker for muscle tissue. Coexpression of desmin and vimentin has been reported in muscular structures, including chicken myoblasts during myogenesis, aortic smooth muscle cells and vascular smooth muscle cells, and vimentin and a-actin in vascular smooth muscle cells.
Efficient adult skeletal muscle regeneration in mice deficient in p38β, p38γ and p38δ MAP kinases
Published in Cell Cycle, 2008
Vanessa Ruiz-Bonilla, Eusebio Perdiguero, Lionel Gresh, Antonio L. Serrano, Mònica Zamora, Pedro Sousa-Victor, Mercè Jardí, Erwin F. Wagner, Pura Muñoz-Cánoves
Adult skeletal muscle is a very stable tissue containing a small population of myofiber-associated quiescent satellite cells compared with late embryonic/neonatal skeletal muscle, which contains highly proliferating myoblasts and small actively growing myofibers, suggesting that specific regulatory pathways may control myogenesis at distinct developmental stages. The p38 MAPK signaling pathway is central for myogenesis, based on studies using immortalized and neonatal primary myoblasts in vitro. However, the contribution of this pathway to adult myogenesis has never been investigated. Four p38 isoforms (p38α, p38β, p38γ and p38δ) exist in mammalian cells, being p38α and p38γ the most abundantly expressed isoforms in adult skeletal muscle. Given the embryonic/neonatal lethality of p38α-deficient mice, here we investigate the relative contribution of p38β, p38γ and p38δ to adult myogenesis. Regeneration and myofiber growth of adult muscle proceeds with similar efficiency in mice lacking p38β, p38γ and p38δ as in wild-type control mice. In agreement with this, there is no difference in adult satellite cell behavior in vitro among the different genotypes. Importantly, the pattern of p38 activation (ascribed to p38α) remains unperturbed during satellite myogenesis in vitro and adult muscle regeneration in wild type and p38β-, p38γ- and p38δ-deficient mice, rendering p38α as the essential p38 isoform sustaining adult myogenesis. This study constitutes the first analysis addressing the functionality of p38β, p38γ and p38δ in satellite cell-dependent adult muscle regeneration and growth.
Histone variants in skeletal myogenesis
Published in Epigenetics, 2021
Nandini Karthik, Reshma Taneja
ABSTRACT Histone variants regulate chromatin accessibility and gene transcription. Given their distinct properties and functions, histone varint substitutions allow for profound alteration of nucleosomal architecture and local chromatin landscape. Skeletal myogenesis driven by the key transcription factor MyoD is characterized by precise temporal regulation of myogenic genes. Timed substitution of variants within the nucleosomes provides a powerful means to ensure sequential expression of myogenic genes. Indeed, growing evidence has shown H3.3, H2A.Z, macroH2A, and H1b to be critical for skeletal myogenesis. However, the relative importance of various histone variants and their associated chaperones in myogenesis is not fully appreciated. In this review, we summarize the role that histone variants play in altering chromatin landscape to ensure proper muscle differentiation. The temporal regulation and cross talk between histones variants and their chaperones in conjunction with other forms of epigenetic regulation could be critical to understanding myogenesis and their involvement in myopathies.
Genetic manipulations reveal dynamic cell and gene functions: Cre-ating a new view of myogenesis
Published in Cell Cycle, 2009
David A. Hutcheson, Gabrielle Kardon
Development of multicellular organisms is temporally and spatially complex. The Cre/loxP and Flp/FRT systems for genetic manipulation in mammals now enable researchers to explicitly examine in vivo the temporal and spatial role of cells and genes during development via cell lineage and ablation studies and conditional gene inactivation and activation. Recently we have used these methods to genetically dissect the role of Pax3+ and Pax7+ progenitor populations and the function of β-catenin, an important regulator of myogenesis, in vertebrate limb myogenesis. Our lineage and ablation studies of Pax3+ and Pax7+ progenitors revealed surprising insights into myogenesis not apparent from Pax3 and Pax7 expression and functional studies. In addition, conditional inactivation and activation of β-catenin in different progenitor populations and their progeny demonstrated that β-catenin plays several cell-autonomous roles in myogenesis. Our studies highlight the hierarchical (i.e. genes versus cells), temporal, and spatial complexity of development and demonstrate that manipulations of both cells and genes will be required to obtain a full understanding of the development of multicellular organisms.
Related Knowledge Centers
- Embryo
- Extracellular Matrix
- Fibroblast Growth Factor
- Fibronectin
- Calcium
- Myocyte
- Metalloproteinase