Histochemical differentiation of skeletal muscle in foetal and newborn mice

Development ◽  
1964 ◽  
Vol 12 (4) ◽  
pp. 759-767
Author(s):  
C. Wirsén ◽  
K. S. Larsson
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Good Deal ◽  
Fibre Types ◽  
Muscle Bundle ◽  
Adult Skeletal Muscle ◽  
Newborn Mice ◽  
Longitudinal Splitting ◽  
Morphological Criteria ◽  
New Generation

In earlier investigations of muscle development, morphological criteria, such as diameter and staining with routine methods, have been used for classifying different fibre types. In human foetal muscle three fibre sizes are seen from the 15th week (Cuajunco, 1942). The largest fibres seem to be the centre of each primary muscle bundle. They were denoted as B fibres by Wohlfart (1937), who considered that they were also functionally different from the smaller ones forming around them. Tello (1922) and Cuajunco (1942) supported the widely held opinion that the smaller fibres are formed from the larger ones by longitudinal splitting. However, Couteaux (1941) claimed that the small fibres belong to a new generation differentiating from interstitial cells. Histochemical studies on foetal muscle are rare. However, during the last years a good deal of work has been carried out on the histochemistry of adult skeletal muscle.

scholarly journals DNA Methylation in Skeletal Muscle Stem Cell Specification, Proliferation, and Differentiation

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Rhianna C. Laker ◽  
James G. Ryall
Keyword(s):  
Skeletal Muscle ◽  
Dna Methylation ◽  
Stem Cells ◽  
Stem Cell ◽  
Muscle Development ◽  
Epigenetic Modification ◽  
Later Life ◽  
Muscle Stem Cell ◽  
Adult Skeletal Muscle ◽  
Muscle Stem Cells

An unresolved and critically important question in skeletal muscle biology is how muscle stem cells initiate and regulate the genetic program during muscle development. Epigenetic dynamics are essential for cellular development and organogenesis in early life and it is becoming increasingly clear that epigenetic remodeling may also be responsible for the cellular adaptations that occur in later life. DNA methylation of cytosine bases within CpG dinucleotide pairs is an important epigenetic modification that reduces gene expression when located within a promoter or enhancer region. Recent advances in the field suggest that epigenetic regulation is essential for skeletal muscle stem cell identity and subsequent cell development. This review summarizes what is currently known about how skeletal muscle stem cells regulate the myogenic program through DNA methylation, discusses a novel role for metabolism in this process, and addresses DNA methylation dynamics in adult skeletal muscle in response to physical activity.

scholarly journals Expression and Functional Analyses of Dlk1 in Muscle Stem Cells and Mesenchymal Progenitors during Muscle Regeneration

2019 ◽  
Vol 20 (13) ◽  
pp. 3269 ◽  
Author(s):  
Lidan Zhang ◽  
Akiyoshi Uezumi ◽  
Takayuki Kaji ◽  
Kazutake Tsujikawa ◽  
Ditte Caroline Andersen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Stem Cells ◽  
Muscle Mass ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Adult Skeletal Muscle ◽  
Fat Accumulation ◽  
Muscle Stem Cells ◽  
Mesenchymal Progenitors ◽  
Regeneration Processes

Delta like non-canonical Notch ligand 1 (Dlk1) is a paternally expressed gene which is also known as preadipocyte factor 1 (Pref−1). The accumulation of adipocytes and expression of Dlk1 in regenerating muscle suggests a correlation between fat accumulation and Dlk1 expression in the muscle. Additionally, mice overexpressing Dlk1 show increased muscle weight, while Dlk1-null mice exhibit decreased body weight and muscle mass, indicating that Dlk1 is a critical factor in regulating skeletal muscle mass during development. The muscle regeneration process shares some features with muscle development. However, the role of Dlk1 in regeneration processes remains controversial. Here, we show that mesenchymal progenitors also known as adipocyte progenitors exclusively express Dlk1 during muscle regeneration. Eliminating developmental effects, we used conditional depletion models to examine the specific roles of Dlk1 in muscle stem cells or mesenchymal progenitors. Unexpectedly, deletion of Dlk1 in neither the muscle stem cells nor the mesenchymal progenitors affected the regenerative ability of skeletal muscle. In addition, fat accumulation was not increased by the loss of Dlk1. Collectively, Dlk1 plays essential roles in muscle development, but does not greatly impact regeneration processes and adipogenic differentiation in adult skeletal muscle regeneration.

scholarly journals Pannexin 1 Regulates Skeletal Muscle Regeneration by Promoting Bleb-Based Myoblast Migration and Fusion Through a Novel Lipid Based Signaling Mechanism

2021 ◽  
Vol 9 ◽  
Author(s):  
Katia Suarez-Berumen ◽  
Henry Collins-Hooper ◽  
Anastasia Gromova ◽  
Robyn Meech ◽  
Alessandra Sacco ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Muscle Development ◽  
Myogenic Differentiation ◽  
Skeletal Muscle Regeneration ◽  
Stem Cell Population ◽  
Amoeboid Movement ◽  
Paracrine Signaling ◽  
Signaling Mechanism ◽  
Adult Skeletal Muscle

Adult skeletal muscle has robust regenerative capabilities due to the presence of a resident stem cell population called satellite cells. Muscle injury leads to these normally quiescent cells becoming molecularly and metabolically activated and embarking on a program of proliferation, migration, differentiation, and fusion culminating in the repair of damaged tissue. These processes are highly coordinated by paracrine signaling events that drive cytoskeletal rearrangement and cell-cell communication. Pannexins are a family of transmembrane channel proteins that mediate paracrine signaling by ATP release. It is known that Pannexin1 (Panx1) is expressed in skeletal muscle, however, the role of Panx1 during skeletal muscle development and regeneration remains poorly understood. Here we show that Panx1 is expressed on the surface of myoblasts and its expression is rapidly increased upon induction of differentiation and that Panx1–/– mice exhibit impaired muscle regeneration after injury. Panx1–/– myoblasts activate the myogenic differentiation program normally, but display marked deficits in migration and fusion. Mechanistically, we show that Panx1 activates P2 class purinergic receptors, which in turn mediate a lipid signaling cascade in myoblasts. This signaling induces bleb-driven amoeboid movement that in turn supports myoblast migration and fusion. Finally, we show that Panx1 is involved in the regulation of cell-matrix interaction through the induction of ADAMTS (Disintegrin-like and Metalloprotease domain with Thrombospondin-type 5) proteins that help remodel the extracellular matrix. These studies reveal a novel role for lipid-based signaling pathways activated by Panx1 in the coordination of myoblast activities essential for skeletal muscle regeneration.

scholarly journals The Chromatin Remodeler Mi2/CHD4 is Required in Skeletal Muscle Stem Cells for Normal Muscle Development and Regeneration

2020 ◽  
Author(s):  
Assia Derfoul ◽  
Iago Pinal-Fernandez ◽  
Wilson Huang ◽  
Cassie Parks ◽  
Katherine Pak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Muscle Development ◽  
Cross Sectional ◽  
Adult Skeletal Muscle ◽  
Altered Expression ◽  
Muscle Stem Cells ◽  
Embryonic Myogenesis ◽  
Skeletal Muscle Stem Cells

Abstract The chromodomain helicase and DNA binding 4 (CHD4) protein is upregulated in regenerating myofibers. To define the role of CHD4 in muscle differentiation and regeneration, we generated mice with CHD4 ablated in muscle satellite cells (SCs). Embryonic day 18.5 CHD4 KO mice are non-viable, with atrophic intercostal and back muscles and altered expression of muscle contraction genes. Tamoxifen-inducible conditional CHD4 KO in adult mouse SCs diminished myoblast proliferation, induced premature differentiation, and altered expression of muscle contraction genes at the myotube stage. Following cardiotoxin–induced muscle injury, CHD4 KO regenerating myofibers had reduced cross-sectional area. ChIP-Seq analysis revealed that CHD4 binds actin a1, Wnt and b-catenin genes, which are known to play roles in the regulation of myogenesis. Together, our results suggest an important role for CHD4 in the control of embryonic myogenesis, SC differentiation, and the control of muscle fiber size in adult skeletal muscle during regeneration.

Alterations in Ultrastructure of Skeletal Muscle From Newborn Guinea Pigs Following in Utero Exposure to Ethanol

1985 ◽  
Vol 43 ◽  
pp. 686-687
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie ◽  
T.B. Cole
Keyword(s):  
Skeletal Muscle ◽  
Guinea Pigs ◽  
Muscle Development ◽  
In Utero ◽  
Ethanol Exposure ◽  
Prenatally Exposed ◽  
Chronic Alcoholic ◽  
Test Kit ◽  
Food And Water Intake ◽  
Post Intubation

Ultrastructural alterations of skeletal muscle have been observed in adult chronic alcoholic patients. However, no such study has been performed on individuals prenatally exposed to ethanol. In order to determine if ethanol exposure in utero in the latter stages of muscle development was deleterious, skeletal muscle was obtained from newborn guinea pigs treated in the following manner. Six Hartly strain pregnant guinea pigs were randomly assigned to either the ethanol or the pair-intubated groups. Twice daily the 3 ethanol-treated animals were intubated with Ensure (Ross Laboratories) liquid diet containing 30% ethanol (6g/Kg pre-pregnant body weight per day) from day 35 of gestation until parturition at day 70±1 day. Serum ethanol levels were determined at 1 hour post-intubation by the Sigma alcohol test kit. For pair-intubation the Ensure diet contained sucrose substituted isocalorically for ethanol. Both food and water intake were monitored.

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