scholarly journals Differential distribution of ryanodine receptor type 3 (RyR3) gene product in mammalian skeletal muscles

1996 ◽  
Vol 316 (1) ◽  
pp. 19-23 ◽  
Author(s):  
Antonio CONTI ◽  
L. GORZA ◽  
Vincenzo SORRENTINO
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Gene Product ◽  
Skeletal Muscles ◽  
Mammalian Species ◽  
Diaphragm Muscle ◽  
Muscle Fibres ◽  
Abdominal Muscles ◽  
Mammalian Skeletal Muscle ◽  
Specific Subset

Activation of intracellular Ca2+-release channels/ryanodine receptors (RyRs) is a fundamental step in the regulation of muscle contraction. In mammalian skeletal muscle, Ca2+-release channels containing the type 1 isoform of RyR (RyR1) open to release Ca2+ from the sarcoplasmic reticulum (SR) upon stimulation by the voltage-activated dihydropyridine receptor on the T-tubule/plasma membrane. In addition to RyR1, low levels of the mRNA of the RyR3 isoform have been recently detected in mammalian skeletal muscles. Here we report data on the distribution of the RyR3 gene product in mammalian skeletal muscles. Western-blot analysis of SR of individual muscles indicated that, at variance with the even distribution of the RyR1 isoform, the RyR3 content varies among different muscles, with relatively higher amounts being detected in diaphragm and soleus, and lower levels in abdominal muscles and tibialis anterior. In these muscles RyR3 was localized in the terminal cisternae of the SR. No detectable levels of RyR3 were observed in the extensor digitorum longus. Preferential high content of RyR3 in the diaphragm muscle was observed in several mammalian species. In situ hybridization analysis demonstrated that RyR3 transcripts are not restricted to a specific subset of skeletal-muscle fibres. Differential utilization of the RyR3 isoform in skeletal muscle may be relevant to the modulation of Ca2+ release with respect to specific muscle-contraction properties.

scholarly journals Skeletal Muscles: Insight into Embryonic Development, Satellite Cells, Histology, Ultrastructure, Innervation, Contraction and Relaxation, Causes, Pathophysiology, and Treatment of Volumetric Muscle I

2021 ◽  
Vol 2 (4) ◽  
pp. 01-17
Author(s):  
Azab Azab
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Embryonic Development ◽  
Satellite Cells ◽  
Skeletal Muscles ◽  
Muscle Fibres ◽  
Mammalian Skeletal Muscle ◽  
Ability To Regenerate ◽  
Contraction And Relaxation ◽  
Skeletal Muscle Fibres

Background: Skeletal muscles are attached to bone and are responsible for the axial and appendicular movement of the skeleton and for maintenance of body position and posture. Objectives: The present review aimed to high light on embryonic development of skeletal muscles, histological and ultrastructure, innervation, contraction and relaxation, causes, pathophysiology, and treatment of volumetric muscle injury. The heterogeneity of the muscle fibers is the base of the flexibility which allows the same muscle to be used for various tasks from continuous low-intensity activity, to repeated submaximal contractions, and to fast and strong maximal contractions. The formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts. As growth of the muscle fibers continues, aggregation into bundles occurs, and by birth, myoblast activity has ceased. Satellite cells (SCs), have single nuclei and act as regenerative cells. Satellite cells are the resident stem cells of skeletal muscle; they are considered to be self-renewing and serve to generate a population of differentiation-competent myoblasts that will participate as needed in muscle growth, repair, and regeneration. Based on various structural and functional characteristics, skeletal muscle fibres are classified into three types: Type I fibres, Type II-B fibres, and type II-A fibres. Skeletal muscle fibres vary in colour depending on their content of myoglobin. Each myofibril exhibits a repeating pattern of cross-striations which is a product of the highly ordered arrangement of the contractile proteins within it. The parallel myofibrils are arranged with their cross-striations in the register, giving rise to the regular striations seen with light microscopy in longitudinal sections of skeletal muscle. Each skeletal muscle receives at least two types of nerve fibers: motor and sensory. Striated muscles and myotendinous junctions contain sensory receptors that are encapsulated proprioceptors. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. During muscle contraction, the thin filaments slide past the thick filaments, as proposed by Huxley's sliding filament theory. In response to a muscle injury, SCs are activated and start to proliferate; at this stage, they are often referred to as either myogenic precursor cells (MPC) or myoblasts. In vitro, evidence has been presented that satellite cells can be pushed towards the adipogenic and osteogenic lineages, but contamination of such cultures from non-myogenic cells is sometimes hard to dismiss as the underlying cause of this observed multipotency. There are, however, other populations of progenitors isolated from skeletal muscle, including endothelial cells and muscle-derived stem cells (MDSCs), blood-vessel-associated mesoangioblasts, muscle side-population cells, CD133+ve cells, myoendothelial cells, and pericytes. Volumetric muscle loss (VML) is defined as the traumatic or surgical loss of skeletal muscle with resultant functional impairment. It represents a challenging clinical problem for both military and civilian medicine. VML results in severe cosmetic deformities and debilitating functional loss. In response to damage, skeletal muscle goes through a well-defined series of events including; degeneration (1 to 3days), inflammation, and regeneration (3 to 4 weeks), fibrosis, and extracellular matrix remodeling (3 to 6 months).. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. During muscle tissue repair following damage, the degree of damage and the interactions between muscle and the infiltrating inflammatory cells appear to affect the successful outcome of the muscle repair process. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering. Conclusion: It can be concluded that the formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts, by birth myoblast activity has ceased. Satellite cells are considered to be self-renewing, and serve to generate a population of differentiation-competent myoblasts. Skeletal muscle fibres are classified into three types. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. VML results in severe cosmetic deformities and debilitating functional loss. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering.

Plasticity in mammalian skeletal muscle

1977 ◽  
Vol 278 (961) ◽  
pp. 295-305 ◽  
Keyword(s):  
Skeletal Muscle ◽  
Peripheral Nerve ◽  
Motor Nerve ◽  
Contractile Proteins ◽  
Biochemical Changes ◽  
Muscle Fibres ◽  
Mammalian Skeletal Muscle ◽  
Motor Innervation ◽  
Nerve Impulses ◽  
Contractile Characteristics

While it has been recognized for many years that different limb muscles belonging to the same mammal may have markedly differing contractile characteristics, it is only comparatively recently that it has been demonstrated that these differences depend upon the motor innervation. By appropriately changing the peripheral nerve innervating a mammalian skeletal muscle, it is possible to change dramatically the contractile behaviour of the reinnervated muscle. The manner by which the motor innervation determines the nature of a muscle fibre’s contractile machinery is not completely understood, but it appears that the number and pattern of motor nerve impulses reaching the muscle play an important role. The biochemical changes occurring within muscle fibres whose contractile properties have been modified by altered motor innervation include the synthesis of different contractile proteins.

scholarly journals Vesicle budding from endoplasmic reticulum is involved in calsequestrin routing to sarcoplasmic reticulum of skeletal muscles

2004 ◽  
Vol 379 (2) ◽  
pp. 505-512 ◽  
Author(s):  
Alessandra NORI ◽  
Elena BORTOLOSO ◽  
Federica FRASSON ◽  
Giorgia VALLE ◽  
Pompeo VOLPE
Keyword(s):  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Sarcoplasmic Reticulum ◽  
Golgi Complex ◽  
Skeletal Muscles ◽  
Muscle Fibres ◽  
Vesicle Budding ◽  
Er Exit Sites ◽  
Skeletal Muscle Fibres ◽  
Mutant Forms

CS (calsequestrin) is an acidic glycoprotein of the SR (sarcoplasmic reticulum) lumen and plays a crucial role in the storage of Ca2+ and in excitation–contraction coupling of skeletal muscles. CS is synthesized in the ER (endoplasmic reticulum) and is targeted to the TC (terminal cisternae) of SR via mechanisms still largely unknown, but probably involving vesicle transport through the Golgi complex. In the present study, two mutant forms of Sar1 and ARF1 (ADP-ribosylation factor 1) were used to disrupt cargo exit from ER-exit sites and intra-Golgi trafficking in skeletal-muscle fibres respectively. Co-expression of Sar1-H79G (His79→Gly) and recombinant, epitope-tagged CS, CSHA1 (where HA1 stands for nine-amino-acid epitope of the viral haemagglutinin 1), barred segregation of CSHA1 to TC. On the other hand, expression of ARF1-N126I altered the subcellular localization of GM130, a cis-medial Golgi protein in skeletal-muscle fibres and myotubes, without interfering with CSHA1 targeting to either TC or developing SR. Thus active budding from ER-exit sites appears to be involved in CS targeting and routing, but these processes are insensitive to modification of intracellular vesicle trafficking and Golgi complex disruption caused by the mutant ARF1-N126I. It also appears that CS routing from ER to SR does not involve classical secretory pathways through ER–Golgi intermediate compartments, cis-medial Golgi and trans-Golgi network.

Twitchin can regulate the ATPase cycle of actomyosin in a phosphorylation-dependent manner in skinned mammalian skeletal muscle fibres

2012 ◽  
Vol 521 (1-2) ◽  
pp. 1-9 ◽  
Author(s):  
Stanislava V. Avrova ◽  
Nikita A. Rysev ◽  
Oleg S. Matusovsky ◽  
Nikolay S. Shelud’ko ◽  
Yurii S. Borovikov
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibres ◽  
Mammalian Skeletal Muscle ◽  
Dependent Manner ◽  
Skeletal Muscle Fibres

scholarly journals Effects of tetracaine on sarcoplasmic calcium release in mammalian skeletal muscle fibres

1999 ◽  
Vol 515 (3) ◽  
pp. 843-857 ◽  
Author(s):  
László Csernoch ◽  
Péter Szentesi ◽  
Sándor Sárközi ◽  
Csaba Szegedi ◽  
István Jona ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Calcium Release ◽  
Muscle Fibres ◽  
Mammalian Skeletal Muscle ◽  
Skeletal Muscle Fibres

scholarly journals Increase in Subcellular GSK-3 Clusters in Insulin- and Adrenaline-treated Differentiated Rat Skeletal Muscle Fibres

2020 ◽  
Author(s):  
Katja Fink ◽  
Mateja Lobe Prebil ◽  
Nina Vardjan ◽  
Jorgen Jensen ◽  
Robert Zorec ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Metabolic Regulation ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase 3 ◽  
Muscle Fibres ◽  
Optical Section ◽  
Rat Skeletal Muscle ◽  
Average Size ◽  
Skeletal Muscle Fibres

Glycogen synthase kinase 3 (GSK-3) plays an important role in metabolic regulation in skeletal muscles, and both insulin and adrenaline stimulate   GKS-3 phosphorylation. The aim of the present study was to study the effect of insulin and adrenaline on GSK-3 localisation in skeletal muscles.We characterized subcellular localization of (GSK-3) signal protein in fully differentiated muscle fibre by immunofluorescence and confocal microscopy. We stimulated muscle fibres with insulin and/or adrenaline. Images were analysed by segmentation of single central optical section of the muscle.We found GSK-3 to be localised in clusters. The number of GSK-3 clusters and their average size were increased after stimulation with insulin and/or adrenaline. Average GSK-3 particle size is linearly related to their quantity.We conclude that subcellular GSK-3 in isolated skeletal muscle fibres is localized in clusters and clustering increased after stimulation with insulin and/or adrenaline.

scholarly journals Gambaran makroskopik dan mikroskopik otot skelet pada hewan coba postmortem

2016 ◽  
Vol 4 (2) ◽  
Author(s):  
Gabriella B. Nelwan ◽  
Sunny Wangko ◽  
Taufik F. Pasiak
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Interval Estimation ◽  
Postmortem Interval ◽  
Postmortem Changes ◽  
Muscle Fibres ◽  
Normal Muscle ◽  
Time Intervals ◽  
Death Time ◽  
Microscopic Change

Abstract: To make pathologists and law personnel aware of the importance of postmortem interval, published studies have reported a lot of methods for estimation of postmortem interval estimation of the remains. This study was aimed to obtain macroscopic and microscopic postmortem changes of skeletal muscle of two domestic pigs weighed 20 kg. This was a descriptive observational study. After the pigs were killed, death time, ambient temperature and humadity were noted. Postmortem evaluation were done at several time intervals, as follows: 30 minutes, 1 hour, 2 hours, 3 hours, 4 hours, 5 hours, 6 hours, 9 hours, 12 hours, 15 hours, 18 hours, 21 hours, 24 hours, 30 hours, 36 hours, 42 hours, and 48 hours. The results showed that at 2 hours after death, the skeletal muscle became pale and soft progressively. The earliest microscopic change was identified at 30 minutes postmortem as pyknotic nuclei of skeletal muscles followed by hydrophic degeneration of muscle fibers and congestion of muscle tisue. At 12 hours until 48 hours postmortem, all microscopic changes became more distinct and widely distributed in nearly all muscle fibres. Albeit, the striated pattern and some normal muscle fibres could still be identified until 48 hours postmortem.Conclusion: Macroscopic changes could be identified the earliest at 2 hours postmortem and microscopic changes could be identified at 30 minutes postmortem.Keywords: macroscopic, microscopic, skeletal muscle, postmortem changes Abstrak: Para peneliti telah banyak menggunakan metode-metode tertentu untuk membuat para penegak hukum dan ahli patologis lainnya memahami pentingnya penentuan jarak waktu kematian. Penelitian ini bertujuan untuk mengetahui gambaran perubahan makroskopik dan mikroskopik postmortem pada otot skelet hewan coba babi dengan massa tubuh lebih kurang 20 kg. Jenis penelitian ialah deskriptif observasional. Hewan coba dimatikan dengan cara ditusuk di bagian jantung, selanjutnya waktu kematian, suhu dan kelembaban ruangan dicatat. Otot skelet diamati pada beberapa interval waktu setelah kematian: 30 menit, 1 jam, 2 jam, 3 jam, 4 jam, 5 jam, 6 jam, 9 jam, 12 jam, 15 jam, 18 jam, 21 jam, 24 jam 30 jam, 36 jam, 42 jam dan 48 jam. Hasil penelitian mendapatkan bahwa otot skelet menjadi pucat dan lunak setelah 2 jam postmortem secara progresif. Pada 1 jam postmortem, tampak serat otot mengalami kongesti dan degenerasi hidropik. Perubahan mikroskopik tersebut menjadi lebih nyata dan tersebar luas di sebagian besar serat otot pada 12 jam sampai 48 postmortem. Walaupun demikian, corak seran lintang dan sebagian kecil serat otot masih tampak normal sampai 48 jam postmortem. Simpulan: Perubahan makroskopik telah dapat diidentifikasi pada 2 jam postmortem sedangkan perubahan mikroskopik mulai dapat diidentifikasi pada 30 menit postmortem.Kata kunci: makroskopik, mikroskopik, otot skelet, perubahan setelah kematian

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