scholarly journals A role of tensin in skeletal-muscle regeneration

2001 ◽  
Vol 356 (3) ◽  
pp. 737-745 ◽  
Author(s):  
Akiko ISHII ◽  
S. Hao LO
Keyword(s):  
Skeletal Muscle ◽  
Knockout Mice ◽  
Muscle Regeneration ◽  
Fold Increase ◽  
Skeletal Muscle Regeneration ◽  
Muscle Fibres ◽  
Double Labelling ◽  
Wild Type ◽  
Associated Proteins

Regeneration of skeletal muscle requires the activation, proliferation, differentiation and fusion of satellite cells to generate new muscle fibres. This study was designed to determine the role of tensin in this process. Cardiotoxin was used to induce regeneration in the anterior tibial muscles of tensin-knockout and wild-type mice. From histological analysis, we found that the regeneration process lasted longer in knockout than in wild-type mice. To investigate the mechanism involved in this delay, we examined each regeneration step in animals and cultured primary cells. We found fewer proliferating myogenic cells identified by bromodeoxyuridine and desmin double labelling in knockout mice on the first 2 days after injury. Expression of myosin, paxillin, dystrophin and dystrophin-associated proteins were delayed in knockout mice. Withdrawal from the cell cycle was less efficient in isolated knockout myoblasts, and the fusion capacity was reduced in these cells as well. These defects in regeneration most likely contributed to the 9-fold increase of centrally nucleated fibres occurring in the non-injected knockout mice. Our results demonstrated clearly that tensin plays a role in skeletal-muscle regeneration.

scholarly journals Alteration of Sarcoplasmic ReticulumCa2+Release in Skeletal Muscle from Calpain 3-Deficient Mice

2009 ◽  
Vol 2009 ◽  
pp. 1-12 ◽  
Author(s):  
Govindan Dayanithi ◽  
Isabelle Richard ◽  
Cédric Viero ◽  
Elsa Mazuc ◽  
Sylvie Mallie ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Cellular Differentiation ◽  
Cyclopiazonic Acid ◽  
Skeletal Muscle Regeneration ◽  
Muscular Dystrophies ◽  
Wild Type ◽  
Calpain 3 ◽  
Deficient Mice

Mutations ofCa2+-activated proteases (calpains) cause muscular dystrophies. Nevertheless, the specific role of calpains inCa2+signalling during the onset of dystrophies remains unclear. We investigatedCa2+handling in skeletal cells from calpain 3-deficient mice.[Ca2+]iresponses to caffeine, a ryanodine receptor (RyR) agonist, were decreased in −/− myotubes and absent in −/− myoblasts. The −/− myotubes displayed smaller amplitudes of theCa2+transients induced by cyclopiazonic acid in comparison to wild type cells. Inhibition of L-typeCa2+channels (LCC) suppressed the caffeine-induced[Ca2+]iresponses in −/− myotubes. Hence, the absence of calpain 3 modifies the sarcoplasmic reticulum (SR)Ca2+release, by a decrease of the SR content, an impairment of RyR signalling, and an increase of LCC activity. We propose that calpain 3-dependent proteolysis plays a role in activating support proteins of intracellularCa2+signalling at a stage of cellular differentiation which is crucial for skeletal muscle regeneration.

scholarly journals The Role of Metabolic Remodeling in Macrophage Polarization and Its Effect on Skeletal Muscle Regeneration

2019 ◽  
Vol 30 (12) ◽  
pp. 1553-1598 ◽  
Author(s):  
Francesca De Santa ◽  
Laura Vitiello ◽  
Alessio Torcinaro ◽  
Elisabetta Ferraro
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Macrophage Polarization ◽  
Skeletal Muscle Regeneration ◽  
Metabolic Remodeling

Urokinase-dependent plasminogen activation is required for efficient skeletal muscle regeneration in vivo

Blood ◽  
2001 ◽  
Vol 97 (6) ◽  
pp. 1703-1711 ◽  
Author(s):  
Frederic Lluı́s ◽  
Josep Roma ◽  
Mònica Suelves ◽  
Maribel Parra ◽  
Gloria Aniorte ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasminogen Activator ◽  
Muscle Regeneration ◽  
Plasminogen Activators ◽  
Skeletal Muscle Regeneration ◽  
Plasminogen Activation ◽  
Wild Type ◽  
Type Plasminogen Activator ◽  
Deficient Mice

Plasminogen activators urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA) are extracellular proteases involved in various tissue remodeling processes. A requirement for uPA activity in skeletal myogenesis was recently demonstrated in vitro. The role of plasminogen activators in skeletal muscle regeneration in vivo in wild-type, uPA-deficient, and tPA-deficient mice is investigated here. Wild-type and tPA−/− mice completely repaired experimentally damaged skeletal muscle. In contrast, uPA−/− mice had a severe regeneration defect, with decreased recruitment of blood-derived monocytes to the site of injury and with persistent myotube degeneration. In addition, uPA-deficient mice accumulated fibrin in the degenerating muscle fibers; however, the defibrinogenation of uPA-deficient mice resulted in a correction of the muscle regeneration defect. A similar severe regeneration deficit with persistent fibrin deposition was also reproducible in plasminogen-deficient mice after injury, suggesting that fibrinolysis by uPA-mediated plasminogen activation plays a fundamental role in skeletal muscle regeneration. In conclusion, the uPA-plasmin system is identified as a critical component of the mammalian skeletal muscle regeneration process, possibly because it prevents intramuscular fibrin accumulation and contributes to the adequate inflammatory response after injury. These studies demonstrate the requirement of an extracellular proteolytic cascade during muscle regeneration in vivo.

The Potential Role of Insulin-Like Growth Factors in Skeletal Muscle Regeneration

1996 ◽  
Vol 21 (4) ◽  
pp. 236-250 ◽  
Author(s):  
Jamie MacGregor ◽  
Wade S. Parkhouse
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Growth Factors ◽  
Muscle Regeneration ◽  
Potential Role ◽  
Tissue Growth ◽  
Skeletal Muscle Regeneration ◽  
Tissue Type ◽  
Insulin Like Growth Factors

The role of the insulin-like growth factors I and II (IGF-I and IGF-II), previously known as the somatomedins, in general growth and development of various tissues has been known for many years. Thought of exclusively as endocrine factors produced by the liver, and under the control of growth hormone, the somatomedins were known as the intermediaries by which growth hormone exerted its cellular effects during tissue growth and maturation. Eventually it was discovered that virtually every tissue type is capable of autocrine production of the IGFs, and their involvement in skeletal muscle tissue repair and regeneration became apparent. Recent advances in technology have allowed the characterisation of many of the different growth factors believed to play a role in muscle regeneration, and experimental manipulations of cells in culture have provided insight into the effects of the various growth factors on the myoblast. This paper explores the potential role of the IGFs in skeletal muscle regeneration. A critical role of IGF-II in terminal differentiation of proliferating muscle precurser cells following injury is proposed. Key words: growth factors, myogenesis, skeletal muscle regeneration

scholarly journals The role of TGF-β1 during skeletal muscle regeneration

2017 ◽  
Vol 41 (7) ◽  
pp. 706-715 ◽  
Author(s):  
Kamila Delaney ◽  
Paulina Kasprzycka ◽  
Maria Anna Ciemerych ◽  
Malgorzata Zimowska
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Tgf Β1

Plasmin activity is required for myogenesis in vitro and skeletal muscle regeneration in vivo

Blood ◽  
2002 ◽  
Vol 99 (8) ◽  
pp. 2835-2844 ◽  
Author(s):  
Mònica Suelves ◽  
Roser López-Alemany ◽  
Frederic Lluı́s ◽  
Gloria Aniorte ◽  
Erika Serrano ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Myoblast Fusion ◽  
Skeletal Muscle Regeneration ◽  
Wild Type ◽  
Plasmin Activity ◽  
Type Plasminogen Activator ◽  
Deficient Mice

Abstract Plasmin, the primary fibrinolytic enzyme, has a broad substrate spectrum and is implicated in biologic processes dependent upon proteolytic activity, such as tissue remodeling and cell migration. Active plasmin is generated from proteolytic cleavage of the zymogen plasminogen (Plg) by urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA). Here, we have investigated the role of plasmin in C2C12 myoblast fusion and differentiation in vitro, as well as in skeletal muscle regeneration in vivo, in wild-type and Plg-deficient mice. Wild-type mice completely repaired experimentally damaged skeletal muscle. In contrast, Plg−/− mice presented a severe regeneration defect with decreased recruitment of blood-derived monocytes and lymphocytes to the site of injury and persistent myotube degeneration. In addition, Plg-deficient mice accumulated fibrin in the degenerating muscle fibers; however, fibrinogen depletion of Plg-deficient mice resulted in a correction of the muscular regeneration defect. Because we found that uPA, but not tPA, was induced in skeletal muscle regeneration, and persistent fibrin deposition was also reproducible in uPA-deficient mice following injury, we propose that fibrinolysis by uPA-dependent plasmin activity plays a fundamental role in skeletal muscle regeneration. In summary, we identify plasmin as a critical component of the mammalian skeletal muscle regeneration process, possibly by preventing intramuscular fibrin accumulation and by contributing to the adequate inflammatory response after injury. Finally, we found that inhibition of plasmin activity with α2-antiplasmin resulted in decreased myoblast fusion and differentiation in vitro. Altogether, these studies demonstrate the requirement of plasmin during myogenesis in vitro and muscle regeneration in vivo.

scholarly journals Macrophages in Skeletal Muscle Dystrophies, An Entangled Partner

2021 ◽  
pp. 1-23
Author(s):  
Theret Marine ◽  
Saclier Marielle ◽  
Messina Graziella ◽  
Rossi M.V. Fabio
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Muscle Regeneration ◽  
Genetic Diseases ◽  
Fatty Infiltration ◽  
Skeletal Muscle Regeneration ◽  
Muscular Dystrophies ◽  
Pathogenic Role ◽  
Muscle Remodeling

While skeletal muscle remodeling happens throughout life, diseases that result in its dysfunction are accountable for many deaths. Indeed, skeletal muscle is exceptionally capable to respond to stimuli modifying its homeostasis, such as in atrophy, hypertrophy, regeneration and repair. In particular conditions such as genetic diseases (muscular dystrophies), skeletal muscle’s capacity to remodel is strongly affected and undergoes continuous cycles of chronic damage. This induces scarring, fatty infiltration, as well as loss of contractibility and of the ability to generate force. In this context, inflammation, primarily mediated by macrophages, plays a central pathogenic role. Macrophages contribute as the primary regulators of inflammation during skeletal muscle regeneration, affecting tissue-resident cells such as myogenic cells and endothelial cells, but also fibro-adipogenic progenitors, which are the main source of the fibro fatty scar. During skeletal muscle regeneration their function is tightly orchestrated, while in dystrophies their fate is strongly disturbed, resulting in chronic inflammation. In this review, we will discuss the latest findings on the role of macrophages in skeletal muscle diseases, and how they are regulated.

The Role of Macrophages in Skeletal Muscle Regeneration with Particular Reference to Chemotaxis

1993 ◽  
Vol 207 (2) ◽  
pp. 321-331 ◽  
Author(s):  
T.A. Robertson ◽  
M.A.L. Maley ◽  
M.D. Grounds ◽  
J.M. Papadimitriou
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration

scholarly journals Necdin mediates skeletal muscle regeneration by promoting myoblast survival and differentiation

2007 ◽  
Vol 179 (2) ◽  
pp. 305-319 ◽  
Author(s):  
Daniela Deponti ◽  
Stéphanie François ◽  
Silvia Baesso ◽  
Clara Sciorati ◽  
Anna Innocenzi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Satellite Cell ◽  
Muscle Regeneration ◽  
Muscle Injury ◽  
Muscle Fibers ◽  
Skeletal Muscle Regeneration ◽  
Muscle Degeneration ◽  
Wild Type ◽  
Cell Type

Regeneration of muscle fibers that are lost during pathological muscle degeneration or after injuries is sustained by the production of new myofibers. An important cell type involved in muscle regeneration is the satellite cell. Necdin is a protein expressed in satellite cell–derived myogenic precursors during perinatal growth. However, its function in myogenesis is not known. We compare transgenic mice that overexpress necdin in skeletal muscle with both wild-type and necdin null mice. After muscle injury the necdin null mice show a considerable defect in muscle healing, whereas mice that overexpress necdin show a substantial increase in myofiber regeneration. We also find that in muscle, necdin increases myogenin expression, accelerates differentiation, and counteracts myoblast apoptosis. Collectively, these data clarify the function and mechanism of necdin in skeletal muscle and show the importance of necdin in muscle regeneration.

Delayed angiogenesis and VEGF production in CCR2−/− mice during impaired skeletal muscle regeneration

2007 ◽  
Vol 293 (2) ◽  
pp. R651-R661 ◽  
Author(s):  
Oscar Ochoa ◽  
Dongxu Sun ◽  
Sara M. Reyes-Reyna ◽  
Lindsay L. Waite ◽  
Joel E. Michalek ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Capillary Density ◽  
Skeletal Muscle Regeneration ◽  
Mouse Strains ◽  
Vascular Endothelial ◽  
Wild Type ◽  
Fiber Size ◽  
Cc Chemokine Receptor 2 ◽  
Endothelial Growth Factor

The regulation of vascular endothelial growth factor (VEGF) levels and angiogenic events during skeletal muscle regeneration remains largely unknown. This study examined angiogenesis, VEGF levels, and muscle regeneration after cardiotoxin (CT)-induced injury in mice lacking the CC chemokine receptor 2 (CCR2). Muscle regeneration was significantly decreased in CCR2−/− mice as was the early accumulation of macrophages after injury. In both mouse strains, tissue VEGF was similar at baseline (no injections) and significantly decreased at day 3 post-CT. Tissue VEGF in wild-type (WT) mice was restored within 7 days postinjury but remained significantly reduced in CCR2−/− mice until day 21. Capillary density (capillaries/mm2) within regenerating muscle was maximal in WT mice at day 7 and double that of baseline muscle. In comparison, maximal capillary density in CCR2−/− mice occurred at 21 days postinjury. Maximal capillary density developed concurrent with the restoration of tissue VEGF in both strains. A highly significant, inverse relationship existed between the size of regenerated muscle fibers and capillaries per square millimeter. Although this relationship was comparable in WT and CCR2−/− animals, there was a significant decrease in the magnitude of this response in the absence of CCR2, reflecting the observation that regenerated muscle fiber size in CCR2−/− mice was only 50% of baseline at 42 days postinjury, whereas WT mice had attained baseline fiber size by day 21. Thus CCR2-dependent events in injured skeletal muscle, including impaired macrophage recruitment, contribute to restoration of tissue VEGF levels and the dynamic processes of capillary formation and muscle regeneration.

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