scholarly journals The role of Drp1 in adult skeletal muscle physiology

2020 ◽  
Vol 598 (21) ◽  
pp. 4761-4763
Author(s):  
Valentin Dablainville ◽  
Anthony M. J. Sanchez
Keyword(s):  
Skeletal Muscle ◽  
Muscle Physiology ◽  
Adult Skeletal Muscle

scholarly journals Role of STIM1/ORAI1-mediated store-operated Ca2+ entry in skeletal muscle physiology and disease

Cell Calcium ◽  
2018 ◽  
Vol 76 ◽  
pp. 101-115 ◽  
Author(s):  
Antonio Michelucci ◽  
Maricela García-Castañeda ◽  
Simona Boncompagni ◽  
Robert T. Dirksen
Keyword(s):  
Skeletal Muscle ◽  
Muscle Physiology

scholarly journals FGF-2–dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis

2021 ◽  
Vol 118 (37) ◽  
pp. e2021013118 ◽  
Author(s):  
Sebastian Mathes ◽  
Alexandra Fahrner ◽  
Umesh Ghoshdastider ◽  
Hannes A. Rüdiger ◽  
Michael Leunig ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transcriptional Activation ◽  
Human Skeletal Muscle ◽  
Muscle Growth ◽  
Muscle Cells ◽  
Adeno Associated Virus ◽  
Adult Skeletal Muscle

Aged skeletal muscle is markedly affected by fatty muscle infiltration, and strategies to reduce the occurrence of intramuscular adipocytes are urgently needed. Here, we show that fibroblast growth factor-2 (FGF-2) not only stimulates muscle growth but also promotes intramuscular adipogenesis. Using multiple screening assays upstream and downstream of microRNA (miR)-29a signaling, we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle of aged mice and humans. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1, which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and adeno-associated virus–mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular adipose tissue (IMAT) formation in vivo. Skeletal muscle from human donors aged >75 y versus <55 y showed activation of FGF-2–dependent signaling and increased IMAT. Thus, our data highlights a disparate role of FGF-2 in adult skeletal muscle and reveals a pathway to combat fat accumulation in aged human skeletal muscle.

scholarly journals Role of synemin, an intermediate filament protein, in adult skeletal muscle (1102.25)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Karla Garcia‐Pelagio ◽  
Joaquin Muriel ◽  
Linda Lund ◽  
Meredith Bond ◽  
Robert Bloch
Keyword(s):  
Skeletal Muscle ◽  
Intermediate Filament ◽  
Intermediate Filament Protein ◽  
Adult Skeletal Muscle ◽  
Filament Protein

scholarly journals CORP: Using transgenic mice to study skeletal muscle physiology

2020 ◽  
Vol 128 (5) ◽  
pp. 1227-1239
Author(s):  
C. Brooks Mobley ◽  
Ivan J. Vechetti ◽  
Taylor R. Valentino ◽  
John J. McCarthy
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Research Program ◽  
Gene Function ◽  
Cell Biology ◽  
Muscle Physiology ◽  
Basic Information ◽  
Adult Skeletal Muscle ◽  
Tissue Specific ◽  
Muscle Research

The development of tissue-specific inducible transgenic mice has provided a powerful tool to study gene function and cell biology in almost any tissue of interest at any given time within the animal’s life. The purpose of this review is to describe how to use two different inducible transgenic systems, the Cre-loxP system and the Tet-ON/OFF system, that can be used to study skeletal muscle physiology. Myofiber- and satellite cell-specific Cre-loxP transgenic mice are described as is how these mice can be used to knockout a gene of interest or to deplete satellite cells in adult skeletal muscle, respectively. A myofiber-specific Tet-ON system is described as is how such mice can be used to overexpress a gene of interest or to label myonuclei. How to effectively breed and genotype the transgenic mice are also described in detail. The hope is this review will provide the basic information necessary to facilitate the incorporation of tissue-specific inducible transgenic mice into a skeletal muscle research program.

Alpha 7 beta 1 integrin is a component of the myotendinous junction on skeletal muscle

1993 ◽  
Vol 106 (2) ◽  
pp. 579-589 ◽  
Author(s):  
Z.Z. Bao ◽  
M. Lakonishok ◽  
S. Kaufman ◽  
A.F. Horwitz
Keyword(s):  
Skeletal Muscle ◽  
Cytoplasmic Domain ◽  
Cross Reactivity ◽  
Myotendinous Junction ◽  
Integrin Subunit ◽  
Adult Skeletal Muscle ◽  
Beta 1 Integrin ◽  
Alpha 7 ◽  
Adhesion Plaque

Immunization against a 70 kDa band that co-purifies with skeletal muscle integrins has resulted in an antibody directed against the avain alpha 7 integrin subunit. The specificity of the antibody was established by patterns of tissue staining and cross-reactivity with antibodies directed against the cytoplasmic domain of the rat alpha 7 cytoplasmic domain. On sections of adult skeletal muscle the alpha 7 integrin was enriched in the myotendinous junction (MTJ). This localization was unique as neither the alpha 1, alpha 3, alpha 5, alpha 6 and alpha v subunit localizes in the myotendinous junction. The distribution of the alpha 7 subunit in the MTJ was examined during embryonic development. alpha 7 expression in the junction is first apparent around embryo day 14 and is almost exclusively at the developing MTJ at this stage. alpha 3 is expressed with distinctive punctate staining around the junctional area in earlier embryos (11-day). The time of appearance of the alpha 7 subunit in the MTJ correlates with the insertion of myofibrils into subsarcolemmal densities and folding of the junctional membrane, suggesting a role of the alpha 7 integrin in this process. Vinculin is present throughout development of the myotendinous junction, suggesting that the alpha 7 integrin recognizes a preformed cytoskeletal structure. The presence of the alpha 7 subunit in the myotendinous junction and the alpha 5 subunit in the adhesion plaque demonstrates a molecular difference between these two adherens junctions. It also points to possible origins of junctional specificity on muscle. Differences between these two junctions were developed further using an antibody against phosphotyrosine (PY20). Phosphotyrosine is thought to participate in the organization and stabilization of adhesions. The focal adhesion and the neuromuscular junction, but not the MTJ, contained proteins phosphorylated on tyrosine.

The role of sphingosine‐1‐phosphate in skeletal muscle: Physiology, mechanisms, and clinical perspectives

2018 ◽  
Vol 234 (7) ◽  
pp. 10047-10059 ◽  
Author(s):  
André V. Cordeiro ◽  
Vagner R. R. Silva ◽  
José R. Pauli ◽  
Adelino S. R. da Silva ◽  
Dennys E. Cintra ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Physiology ◽  
Sphingosine 1 Phosphate

scholarly journals Brain-derived Neurotrophic Factor Regulates Satellite Cell Differentiation and Skeltal Muscle Regeneration

2010 ◽  
Vol 21 (13) ◽  
pp. 2182-2190 ◽  
Author(s):  
Charlene Clow ◽  
Bernard J. Jasmin
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cell ◽  
Satellite Cells ◽  
Neurotrophic Factor ◽  
Cell Function ◽  
Brain Derived Neurotrophic Factor ◽  
Postnatal Growth ◽  
Adult Skeletal Muscle

In adult skeletal muscle, brain-derived neurotrophic factor (BDNF) is expressed in myogenic progenitors known as satellite cells. To functionally address the role of BDNF in muscle satellite cells and regeneration in vivo, we generated a mouse in which BDNF is specifically depleted from skeletal muscle cells. For comparative purposes, and to determine the specific role of muscle-derived BDNF, we also examined muscles of the complete BDNF−/− mouse. In both models, expression of the satellite cell marker Pax7 was significantly decreased. Furthermore, proliferation and differentiation of primary myoblasts was abnormal, exhibiting delayed induction of several markers of differentiation as well as decreased myotube size. Treatment with exogenous BDNF protein was sufficient to rescue normal gene expression and myotube size. Because satellite cells are responsible for postnatal growth and repair of skeletal muscle, we next examined whether regenerative capacity was compromised. After injury, BDNF-depleted muscle showed delayed expression of several molecular markers of regeneration, as well as delayed appearance of newly regenerated fibers. Recovery of wild-type BDNF levels was sufficient to restore normal regeneration. Together, these findings suggest that BDNF plays an important role in regulating satellite cell function and regeneration in vivo, particularly during early stages.

scholarly journals Super-relaxed state of myosin in human skeletal muscle is fiber-type dependent

2020 ◽  
Author(s):  
Lien A. Phung ◽  
Aurora D. Foster ◽  
Mark S. Miller ◽  
Dawn A. Lowe ◽  
David D. Thomas
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Vastus Lateralis ◽  
Epifluorescence Microscopy ◽  
Model Organisms ◽  
Muscle Physiology ◽  
Fiber Types ◽  
Mhc I

AbstractThe myosin super-relaxed state (SRX) in skeletal muscle is hypothesized to play an important role in regulating muscle contractility and thermogenesis in humans, but has only been examined in model organisms. Here we report the first human skeletal muscle SRX measurements, using quantitative epifluorescence microscopy of fluorescent 2’/3’-O-(N-methylanthraniloyl) ATP (mantATP) single-nucleotide turnover. Myosin heavy chain (MHC) isoform expression was determined using gel electrophoresis for each permeabilized vastus lateralis fiber, to allow for novel comparisons of SRX between fiber-types. We find that the fraction of myosin in SRX is less in MHC IIA fibers than in MHC I and IIAX fibers (p = 0.008). ATP turnover of SRX is faster in MHC IIAX fibers compared to MHC I and IIA fibers (p = 0.001). We conclude that SRX biochemistry is measurable in human skeletal muscle, and our data indicate that SRX depends on fiber type as classified by MHC isoform. Extension from this preliminary work would provide further understanding regarding the role of SRX in human muscle physiology.

scholarly journals Role of Protein Arginine Methyltransferases and Inflammation in Muscle Pathophysiology

2021 ◽  
Vol 12 ◽  
Author(s):  
Hyun-Kyung So ◽  
Sunghee Kim ◽  
Jong-Sun Kang ◽  
Sang-Jin Lee
Keyword(s):  
Skeletal Muscle ◽  
Chronic Inflammation ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Current Knowledge ◽  
Arginine Methylation ◽  
Muscle Physiology ◽  
Post Translational Modification ◽  
Protein Arginine Methyltransferases

Arginine methylation mediated by protein arginine methyltransferases (PRMTs) is a post-translational modification of both histone and non-histone substrates related to diverse biological processes. PRMTs appear to be critical regulators in skeletal muscle physiology, including regeneration, metabolic homeostasis, and plasticity. Chronic inflammation is commonly associated with the decline of skeletal muscle mass and strength related to aging or chronic diseases, defined as sarcopenia. In turn, declined skeletal muscle mass and strength can exacerbate chronic inflammation. Thus, understanding the molecular regulatory pathway underlying the crosstalk between skeletal muscle function and inflammation might be essential for the intervention of muscle pathophysiology. In this review, we will address the current knowledge on the role of PRMTs in skeletal muscle physiology and pathophysiology with a specific emphasis on its relationship with inflammation.

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