Role of innervation on the embryonic development of skeletal muscle

1980 ◽  
Vol 210 (3) ◽  
Author(s):  
G.S. Sohal ◽  
R.K. Holt
Keyword(s):  
Skeletal Muscle ◽  
Embryonic Development

scholarly journals Multiple roles of syndecan-4 during myoblast migration

2021 ◽  
Author(s):  
Dániel Becsky
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Cell Migration ◽  
Embryonic Development ◽  
Cell Polarity ◽  
Focal Adhesion ◽  
Muscle Disease ◽  
Satellite Stem Cells ◽  
Migrating Cells

Background and purpose: Cell migration is one of the cornerstones of regeneration processes, as it is necessary for wound healing, and also required for embryonic development, immune system activation, or tumor metastasis formation. Skeletal muscle has a special, advanced dynamism that allows it to adapt to various impacts and recover successfully after an injury, exercise, or muscle disease. Satellite stem cells are activated by local damage during muscle regeneration, and after asymmetric division, myoblasts (i.e., activated satellite cells) migrate to the site of injury, differentiate, and fuse to form muscle fibers. Migration of the cells requires cellular polarization, the creation of leading and trailing edges, as well as the proper orientation and positioning of organelles inside the cell. Efficient migration also requires the presence of an asymmetrical front-to-rear calcium (Ca2+) gradient to regulate focal adhesion assembly and actomyosin contractility. The transmembrane proteoglycan syndecan-4 (SDC4), which is one of the cell surface markers of resting and activated satellite stem cells, is involved in the formation of focal adhesions. Furthermore, SDC4 plays a variety of roles in signal transduction processes, including controlling the function of the small GTPase Rac1 by binding to and inhibiting the activity of T-lymphoma invasion and metastasis-1 (Tiam1), a guanine nucleotide exchange factor for Rac1 (Ras-related C3 botulinum toxin substrate 1) GTPase. Cell migration also requires Rac1-mediated actin remodeling. SDC4 knockout mice are unable to regenerate damaged muscle; however, its underlying precise mechanism is unclear; therefore, our aim was to analyze the role of SDC4 in myoblast migration. Experimental approaches: To achieve SDC4 knockdown, C2C12 murine myoblast cells were transfected stably with plasmids expressing short hairpin RNAs (shRNAs) specific for mouse SDC4 (shSDC4#1 and shSDC4#2) or a scrambled target sequence. To study cell migration, time-lapse images were captured at 37 °C and 5% CO2 using a high-content imaging system for single-cell tracking or wound scratch assay was performed. To evaluate the movement of the single cells, the cell nuclei were tracked with ImageJ and CellTracker software. Super-resolution direct stochastic optical reconstruction microscopy (dSTORM) measurements were performed for the nanoscale analysis of the lamellipodial actin network of the migrating cells. To study the intracellular Ca2+ level, Fluo-4 and Fura Red indicators were applied. Immunofluorescence cytochemistry was performed to analyze the distribution of SDC4, Tiam1, centrosomes, FAK (focal adhesion kinase) or GM130 (anti- Golgi matrix protein of 130 kDa) followed by wide-field fluorescence or confocal microscopy. Image analysis was performed with ImageJ. Rac1 was inhibited by NSC23766 treatment during the measurements (50 µM). Key results: Silencing of SDC4 disrupts the correct polarization of migrating mammalian myoblasts. SDC4 knockdown completely abolished the intracellular Ca2+ gradient, abrogated centrosome reorientation, and thus decreased cell motility, demonstrating the role of SDC4 in cell polarity. Additionally, SDC4 exhibited a polarized distribution during migration. SDC4 knockdown cells exhibited decreases in the total movement distance during migration, maximum and vectorial distances from the starting point, as well as average and maximum cell speeds. Analysis of the dSTORM images of SDC4 knockdown cells revealed nanoscale changes in the actin cytoskeletal architecture, such as decreases in the numbers of branches and individual branch lengths in the lamellipodia of the migrating cells. The Rac1 inhibitor NSC23766 did not restore the migration capacity of SDC4 silenced cells; in fact, it reduced it further. SDC4 knockdown decreased the directional persistence of migration, abrogated the polarized, asymmetric distribution of Tiam1, and reduced the total Tiam1 level of the cells. Conclusion: According to our results, SDC4 affects the migration of C2C12 myoblasts and modulates cell polarity by influencing centrosome positioning, intracellular Ca2+ and Tiam1 distribution. These findings may promote greater understanding the essential role of SDC4 in the embryonic development and postnatal regeneration of skeletal muscle. Given the ubiquitous expression and crucial role of SDC4 in cell migration, we conclude that our findings can facilitate understanding the general role of SDC4 during cell migration.

MIOPATIA MUSCULAR ESQUELÉTICA INDUZIDA PELA INSUFICIÊNCIA CARDÍACA DE ETIOLOGIA HIPERTENSIVA: PAPEL TERAPÊUTICO DO TREINAMENTO FÍSICO AERÓBIOHYPERTENSIVE HEART FAILURE-INDUCED SKELETAL MUSCLE MYOPATHY: THERAPEUTIC ROLE OF AEROBIC EXERCISE TRAININGRESUMOA insuficiência cardíaca (IC) é a via final comum da maioria das doenças que acometem o coração. Entre os fatores de risco conhecidos, a hipertensão arterial (HA) é a doença mais frequentemente associada à IC. Caracterizada pela intolerância ao exercício, a IC promove disfunção cardíaca e alterações intrínsecas musculares envolvidas na redução da capacidade física. Várias anormalidades do músculo esquelético têm sido descritas em pacientes e animais com IC, incluindo atrofia, fibrose, mudança na composição dos tipos de fibras, rarefação microvascular e reduzida capacidade de oxidação. Por outro lado, o treinamento físico aeróbio (TFA) vem sendo utilizado como uma importante terapia não farmacológica para a prevenção e o tratamento da IC; em parte, por melhorar a função endotelial e a perfusão coronária, diminuir a resistência vascular periférica e induzir o remodelamento das células musculares cardíacas e esqueléticas, levando ao aumento da captação de oxigênio e resistência à fadiga. Os mecanismos e vias de sinalização intracelular envolvidas nas anormali

2020 ◽  
Vol 30 (2) ◽  
pp. 239-247
Author(s):  
Bruno Rocha de Avila Pelozin ◽  
◽  
Larissa Ferreira-Santos ◽  
Luis Felipe Rodrigues ◽  
Edilamar Menezes de Oliveira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Aerobic Exercise ◽  
Therapeutic Role ◽  
Insuficiencia Cardiaca

Role of Oxidative Stress and Mitochondrial Dysfunction in Skeletal Muscle in Type 2 Diabetic Patients

2016 ◽  
Vol 22 (18) ◽  
pp. 2650-2656 ◽  
Author(s):  
Noelia Diaz-Morales ◽  
Susana Rovira-Llopis ◽  
Irene Escribano-Lopez ◽  
Celia Bañuls ◽  
Sandra Lopez-Domenech ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

scholarly journals Essential Role of Septin 7 in Skeletal Muscle Structure and Function

2020 ◽  
Vol 118 (3) ◽  
pp. 258a
Author(s):  
Laszlo Csernoch ◽  
Mónika Gönczi ◽  
Zsolt Ráduly ◽  
László Szabó ◽  
Nóra Dobrosi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Essential Role ◽  
Structure And Function ◽  
Muscle Structure ◽  
And Function

Determinants of maximal whole-body fat oxidation in elite cross-country skiers: Role of skeletal muscle mitochondria

2018 ◽  
Vol 28 (12) ◽  
pp. 2494-2504 ◽  
Author(s):  
Sune Dandanell ◽  
Anne-Kristine Meinild-Lundby ◽  
Andreas B. Andersen ◽  
Paul F. Lang ◽  
Laura Oberholzer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Body Fat ◽  
Fat Oxidation ◽  
Whole Body ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria ◽  
Cross Country

scholarly journals Inhibition of Aurora Kinase B activity disrupts development and differentiation of salivary glands

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer K. Shaalan ◽  
Tathyane H. N. Teshima ◽  
Abigail S. Tucker ◽  
Gordon B. Proctor
Keyword(s):  
Cell Cycle ◽  
Embryonic Development ◽  
Salivary Glands ◽  
Aurora Kinase ◽  
Serine Threonine Kinase ◽  
Aurora Kinase B ◽  
Development And Differentiation ◽  
Differentiation Marker ◽  
Key Events

AbstractLittle is known about the key molecules that regulate cell division during organogenesis. Here we determine the role of the cell cycle promoter aurora kinase B (AURKB) during development, using embryonic salivary glands (E-SGs) as a model. AURKB is a serine/threonine kinase that regulates key events in mitosis, which makes it an attractive target for tailored anticancer therapy. Many reports have elaborated on the role of AURKB in neoplasia and cancer; however, no previous study has shown its role during organ development. Our previous experiments have highlighted the essential requirement for AURKB during adult exocrine regeneration. To investigate if AURKB is similarly required for progression during embryonic development, we pharmacologically inhibited AURKB in developing submandibular glands (SMGs) at embryonic day (E)13.5 and E16.5, using the highly potent and selective drug Barasertib. Inhibition of AURKB interfered with the expansion of the embryonic buds. Interestingly, this effect on SMG development was also seen when the mature explants (E16.5) were incubated for 24 h with another cell cycle inhibitor Aphidicolin. Barasertib prompted apoptosis, DNA damage and senescence, the markers of which (cleaved caspase 3, γH2AX, SA-βgal and p21, respectively), were predominantly seen in the developing buds. In addition to a reduction in cell cycling and proliferation of the epithelial cells in response to AURKB inhibition, Barasertib treatment led to an excessive generation of reactive oxygen species (ROS) that resulted in downregulation of the acinar differentiation marker Mist1. Importantly, inhibition of ROS was able to rescue this loss of identity, with Mist1 expression maintained despite loss of AURKB. Together, these data identify AURKB as a key molecule in supporting embryonic development and differentiation, while inhibiting senescence-inducing signals during organogenesis.

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