scholarly journals Desmin Is Essential for the Tensile Strength and Integrity of Myofibrils but Not for Myogenic Commitment, Differentiation, and Fusion of Skeletal Muscle

1997 ◽  
Vol 139 (1) ◽  
pp. 129-144 ◽  
Author(s):  
Zhenlin Li ◽  
Mathias Mericskay ◽  
Onnik Agbulut ◽  
Gillian Butler-Browne ◽  
Lena Carlsson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Structural Integrity ◽  
Weight Bearing ◽  
Repair Process ◽  
Relative Increase ◽  
Null Mutation ◽  
Muscle Formation ◽  
Slow Myosin Heavy Chain ◽  
Cardiac Muscles ◽  
Second Wave

A null mutation was introduced into the mouse desmin gene by homologous recombination. The desmin knockout mice (Des −/−) develop normally and are fertile. However, defects were observed after birth in skeletal, smooth, and cardiac muscles (Li, Z., E. Colucci-Guyon, M. Pincon-Raymond, M. Mericskay, S. Pournin, D. Paulin, and C. Babinet. 1996. Dev. Biol. 175:362–366; Milner, D.J., G. Weitzer, D. Tran, A. Bradley, and Y. Capetanaki. 1996. J. Cell Biol. 134:1255– 1270). In the present study we have carried out a detailed analysis of somitogenesis, muscle formation, maturation, degeneration, and regeneration in Des −/− mice. Our results demonstrate that all early stages of muscle differentiation and cell fusion occur normally. However, after birth, modifications were observed essentially in weight-bearing muscles such as the soleus or continually used muscles such as the diaphragm and the heart. In the absence of desmin, mice were weaker and fatigued more easily. The lack of desmin renders these fibers more susceptible to damage during contraction. We observed a process of degeneration of myofibers, accompanied by macrophage infiltration, and followed by a process of regeneration. These cycles of degeneration and regeneration resulted in a relative increase in slow myosin heavy chain (MHC) and decrease in fast MHC. Interestingly, this second wave of myofibrillogenesis during regeneration was often aberrant and showed signs of disorganization. Subsarcolemmal accumulation of mitochondria were also observed in these muscles. The lack of desmin was not compensated by an upregulation of vimentin in these mice either during development or regeneration. Absence of desmin filaments within the sarcomere does not interfere with primary muscle formation or regeneration. However, myofibrillogenesis in regenerating fibers is often abortive, indicating that desmin may be implicated in this repair process. The results presented here show that desmin is essential to maintain the structural integrity of highly solicited skeletal muscle.

Two structural states of the Z-band in cardiac and skeletal muscle

1989 ◽  
Vol 47 ◽  
pp. 1022-1023
Author(s):  
J.P. Schroeter ◽  
M.A. Goldstein ◽  
J.P. Bretaudiere ◽  
L.H. Michael ◽  
R.L. Sass
Keyword(s):  
Skeletal Muscle ◽  
Cross Section ◽  
Real Space ◽  
Contractile State ◽  
Contour Maps ◽  
False Color ◽  
Grey Scale ◽  
Fourier Filtering ◽  
Cardiac Muscles ◽  
Enhancement Algorithm

We have recently established the existence of two structural states of the Z band lattice in cross section in cardiac as well as in skeletal muscle. The two structural states are related to the contractile state of the muscle. In skeletal muscle at rest, the Z band is in the small square (ss) lattice form, but tetanized muscle exhibits the basket weave (bw) form. In contrast, unstimu- lated cardiac muscle exhibits the bw form, but cardiac muscles exposed to EGTA show the ss form.We have used two-dimensional computer enhancement techniques on digitized electron micrographs to compare each lattice form as it appears in both cardiac and skeletal muscle. Both real space averaging and fourier filtering methods were used. Enhanced images were displayed as grey-scale projections, as contour maps, and in false color.There is only a slight difference between the lattices produced by the two different enhancement techniques. Thus the information presented in these images is not likely to be an artifact of the enhancement algorithm.

Sex differences in the involvement of skeletal and cardiac muscles in myopathic Ano5-/- mice.

2022 ◽  
Author(s):  
Steven Foltz ◽  
Fang Wu ◽  
Nasab Ghazal ◽  
Jennifer Kwong ◽  
H. Criss Hartzell ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Sex Differences ◽  
Meta Analysis ◽  
Elevated Serum ◽  
Research Literature ◽  
Exercise Intolerance ◽  
Membrane Repair ◽  
Recessive Mutations ◽  
Skeletal Muscle Dysfunction ◽  
Cardiac Muscles

Limb-girdle muscular dystrophy R12 (LGMD-R12) is caused by recessive mutations in the Anoctamin-5 gene (ANO5, TMEM16E). Although ANO5 myopathy is not X-chromosome linked, we performed a meta-analysis of the research literature and found that three-quarters of LGMD-R12 patients are males. Females are less likely to present with moderate to severe skeletal muscle and/or cardiac pathology. Because these sex differences could be explained in several ways, we compared males and females in a mouse model of LGMD-R12. This model recapitulates the sex differences in human LGMD-R12. Only male Ano5-/- mice had elevated serum creatine kinase after exercise and exhibited defective membrane repair after laser injury. In contrast, by these measures, female Ano5-/- mice were indistinguishable from wild type. Despite these differences, both male and female Ano5-/- mice exhibited exercise intolerance. While exercise intolerance of male mice can be explained by skeletal muscle dysfunction, echocardiography revealed that Ano5-/- female mice had features of cardiomyopathy that may be responsible for their exercise intolerance. These findings heighten concerns that mutations of ANO5 in humans may be linked to cardiac disease.

scholarly journals AMP-Activated Protein Kinase as a Key Trigger for the Disuse-Induced Skeletal Muscle Remodeling

2018 ◽  
Vol 19 (11) ◽  
pp. 3558 ◽  
Author(s):  
Natalia Vilchinskaya ◽  
Igor Krivoi ◽  
Boris Shenkman
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Histone Deacetylases ◽  
Molecular Mechanisms ◽  
Weight Bearing ◽  
Mammalian Target Of Rapamycin ◽  
Adenosine Monophosphate ◽  
Chain Gene ◽  
Mtorc1 Signaling ◽  
The Impact

Molecular mechanisms that trigger disuse-induced postural muscle atrophy as well as myosin phenotype transformations are poorly studied. This review will summarize the impact of 5′ adenosine monophosphate -activated protein kinase (AMPK) activity on mammalian target of rapamycin complex 1 (mTORC1)-signaling, nuclear-cytoplasmic traffic of class IIa histone deacetylases (HDAC), and myosin heavy chain gene expression in mammalian postural muscles (mainly, soleus muscle) under disuse conditions, i.e., withdrawal of weight-bearing from ankle extensors. Based on the current literature and the authors’ own experimental data, the present review points out that AMPK plays a key role in the regulation of signaling pathways that determine metabolic, structural, and functional alternations in skeletal muscle fibers under disuse.

Alpha-actin and cytochrome c mRNAs in atrophied adult rat skeletal muscle

1988 ◽  
Vol 254 (5) ◽  
pp. C651-C656 ◽  
Author(s):  
P. Babij ◽  
F. W. Booth
Keyword(s):  
Skeletal Muscle ◽  
Cytochrome C ◽  
Muscle Atrophy ◽  
Weight Bearing ◽  
Skeletal Muscle Atrophy ◽  
Rna Content ◽  
Mrna Content ◽  
Fast Twitch Muscle ◽  
Alpha Actin ◽  
Fast Twitch

Specific complementary DNA (cDNA) hybridization probes were used to estimate the levels of alpha-actin and cytochrome c mRNAs and also 18S rRNA in three models of skeletal muscle atrophy. After 7 days of hindlimb suspension, or immobilization, or denervation, protein content decreased 26-32% in all muscles studied except suspended fast-twitch muscle, which lost only half as much protein. alpha-Actin mRNA content decreased 51-66% and cytochrome c mRNA content decreased 42-61% in slow- and fast-twitch muscles in all three models of atrophy. However, total RNA content did not show similar directional changes; RNA content decreased 27-44% in suspended and immobilized muscle but was unchanged in denervated fast-twitch muscle. The results were interpreted to suggest that loss of weight-bearing function of skeletal muscle is a major factor affecting the levels of alpha-actin and cytochrome c mRNAs during muscle atrophy.

Structural Integrity Evaluation of a Reactor Vessel Outlet Nozzle Weld Inlay

2012 ◽  
Author(s):  
N. L. Glunt ◽  
A. Udyawar ◽  
C. K. Ng ◽  
S. E. Marlette
Keyword(s):  
Stress Corrosion ◽  
Stress Corrosion Cracking ◽  
Structural Integrity ◽  
Repair Process ◽  
Reactor Vessel ◽  
Nuclear Industry ◽  
Outlet Nozzle ◽  
Weld Material ◽  
Asme Code ◽  
Primary Water

Nickel-base weldments such as Alloy 82/182 dissimilar metal (DM) butt welds used in Pressurized Water Reactor (PWR) nuclear power plant components have experienced Primary Water Stress Corrosion Cracking (PWSCC), resulting in the need to repair/replace these weldments. The nuclear industry has been actively engaged in inspecting and mitigating these susceptible DM butt welds for the past several years. Full and Optimized Structural Weld Overlay as well as Mechanical Stress Improvement Process (MSIP®) are some of the mitigation/repair processes that have been implemented successfully by the nuclear industry to mitigate PWSCC. Three conditions must exist simultaneously for PWSCC to occur: high tensile stresses, susceptible material and an environment that is conducive to stress corrosion cracking. These mitigation/repair processes are effective in minimizing the potential for future initiation and crack propagation resulting from PWSCC by generating compressive residual stress at the inner surface of the susceptible DM weld. Weld inlay is an alternative mitigation/repair process especially for large bore nozzles such as reactor vessel nozzles. The weld inlay process consists of excavating a small portion of the susceptible weld material at the inside surface of the component and then applying a PWSCC resistant Alloy 52/52M repair weld layer on the inside surface of the component to isolate the susceptible DM weld material from the primary water environment. The design and analysis requirements of the weld inlay are provided in ASME Code Case N-766. This paper provides the structural integrity evaluation results for a typical reactor vessel outlet nozzle weld inlay performed in accordance with the ASME Code Case N-766 design and analysis requirements. The evaluation results demonstrate that weld inlay is also a viable PWSCC mitigation and repair process especially for large bore reactor vessel nozzles.

scholarly journals Mechanism and Functions of Identified miRNAs in Poultry Skeletal Muscle Development – A Review

2019 ◽  
Vol 19 (4) ◽  
pp. 887-904
Author(s):  
Asiamah Amponsah Collins ◽  
Kun Zou ◽  
Zhang Li ◽  
Su Ying
Keyword(s):  
Skeletal Muscle ◽  
Candidate Genes ◽  
Skeletal Muscles ◽  
Muscle Development ◽  
Muscle Growth ◽  
Skeletal Muscle Development ◽  
Single Nucleotide ◽  
Complex Processes ◽  
Muscle Formation ◽  
Gene Regulatory

AbstractDevelopment of the skeletal muscle goes through several complex processes regulated by numerous genetic factors. Although much efforts have been made to understand the mechanisms involved in increased muscle yield, little work is done about the miRNAs and candidate genes that are involved in the skeletal muscle development in poultry. Comprehensive research of candidate genes and single nucleotide related to poultry muscle growth is yet to be experimentally unraveled. However, over a few periods, studies in miRNA have disclosed that they actively participate in muscle formation, differentiation, and determination in poultry. Specifically, miR-1, miR-133, and miR-206 influence tissue development, and they are highly expressed in the skeletal muscles. Candidate genes such as CEBPB, MUSTN1, MSTN, IGF1, FOXO3, mTOR, and NFKB1, have also been identified to express in the poultry skeletal muscles development. However, further researches, analysis, and comprehensive studies should be made on the various miRNAs and gene regulatory factors that influence the skeletal muscle development in poultry. The objective of this review is to summarize recent knowledge in miRNAs and their mode of action as well as transcription and candidate genes identified to regulate poultry skeletal muscle development.

Spaceflight on STS-48 and earth-based unweighting produce similar effects on skeletal muscle of young rats

1993 ◽  
Vol 74 (5) ◽  
pp. 2161-2165 ◽  
Author(s):  
M. E. Tischler ◽  
E. J. Henriksen ◽  
K. A. Munoz ◽  
C. S. Stump ◽  
C. R. Woodman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Extensor Digitorum Longus ◽  
Space Shuttle ◽  
Weight Bearing ◽  
Similar Rate ◽  
Extensor Digitorum ◽  
Hindlimb Suspension ◽  
Albino Rats ◽  
Sprague Dawley ◽  
Ambient Temperatures

Our knowledge of the effects of unweighting on skeletal muscle of juvenile rapidly growing rats has been obtained entirely by using hindlimb-suspension models. No spaceflight data on juvenile animals are available to validate these models of simulated weightlessness. Therefore, eight 26-day-old female Sprague-Dawley albino rats were exposed to 5.4 days of weightlessness aboard the space shuttle Discovery (mission STS-48, September 1991). An asynchronous ground control experiment mimicked the flight cage condition, ambient shuttle temperatures, and mission duration for a second group of rats. A third group of animals underwent hindlimb suspension for 5.4 days at ambient temperatures. Although all groups consumed food at a similar rate, flight animals gained a greater percentage of body mass per day (P < 0.05). Mass and protein data showed weight-bearing hindlimb muscles were most affected, with atrophy of the soleus and reduced growth of the plantaris and gastrocnemius in both the flight and suspended animals. In contrast, the non-weight-bearing extensor digitorum longus and tibialis anterior muscles grew normally. Earlier suspension studies showed that the soleus develops an increased sensitivity to insulin during unweighting atrophy, particularly for the uptake of 2-[1,2–3H]deoxyglucose. Therefore, this characteristic was studied in isolated muscles within 2 h after cessation of spaceflight or suspension. Insulin increased uptake 2.5- and 2.7-fold in soleus of flight and suspended animals, respectively, whereas it increased only 1.6-fold in control animals. In contrast, the effect of insulin was similar among the three groups for the extensor digitorum longus, which provides a control for potential systemic differences in the animals.

scholarly journals Ankrd2 in Mechanotransduction and Oxidative Stress Response in Skeletal Muscle: New Cues for the Pathogenesis of Muscular Laminopathies

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Vittoria Cenni ◽  
Snezana Kojic ◽  
Cristina Capanni ◽  
Georgine Faulkner ◽  
Giovanna Lattanzi
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Stress Response ◽  
Muscular Dystrophy ◽  
Transcriptional Response ◽  
Oxidative Stress Response ◽  
Ankyrin Repeat ◽  
Lamin A ◽  
Cellular Reactive Oxygen Species ◽  
Cardiac Muscles

Ankrd2 (ankyrin repeats containing domain 2) or Arpp (ankyrin repeat, PEST sequence, and proline-rich region) is a member of the muscle ankyrin repeat protein family. Ankrd2 is mostly expressed in skeletal muscle, where it plays an intriguing role in the transcriptional response to stress induced by mechanical stimulation as well as by cellular reactive oxygen species. Our studies in myoblasts from Emery-Dreifuss muscular dystrophy 2, a LMNA-linked disease affecting skeletal and cardiac muscles, demonstrated that Ankrd2 is a lamin A-binding protein and that mutated lamins found in Emery-Dreifuss muscular dystrophy change the dynamics of Ankrd2 nuclear import, thus affecting oxidative stress response. In this review, besides describing the latest advances related to Ankrd2 studies, including novel discoveries on Ankrd2 isoform-specific functions, we report the main findings on the relationship of Ankrd2 with A-type lamins and discuss known and potential mechanisms involving defective Ankrd2-lamin A interplay in the pathogenesis of muscular laminopathies.

scholarly journals Dynamics of Myoblast Transplantation Reveal a Discrete Minority of Precursors with Stem Cell–like Properties as the Myogenic Source

1999 ◽  
Vol 144 (6) ◽  
pp. 1113-1122 ◽  
Author(s):  
Jonathan R. Beauchamp ◽  
Jennifer E. Morgan ◽  
Charles N. Pagel ◽  
Terence A. Partridge
Keyword(s):  
Cell Cycle ◽  
Skeletal Muscle ◽  
Tissue Culture ◽  
Stem Cell ◽  
Genetic Modification ◽  
Muscle Formation ◽  
Myoblast Transplantation ◽  
Dystrophic Mice

Myoblasts, the precursors of skeletal muscle fibers, can be induced to withdraw from the cell cycle and differentiate in vitro. Recent studies have also identified undifferentiated subpopulations that can self-renew and generate myogenic cells (Baroffio, A., M. Hamann, L. Bernheim, M.-L. Bochaton-Pillat, G. Gabbiani, and C.R. Bader. 1996. Differentiation. 60:47–57; Yoshida, N., S. Yoshida, K. Koishi, K. Masuda, and Y. Nabeshima. 1998. J. Cell Sci. 111:769–779). Cultured myoblasts can also differentiate and contribute to repair and new muscle formation in vivo, a capacity exploited in attempts to develop myoblast transplantation (MT) for genetic modification of adult muscle. Our studies of the dynamics of MT demonstrate that cultures of myoblasts contain distinct subpopulations defined by their behavior in vitro and divergent responses to grafting. By comparing a genomic and a semiconserved marker, we have followed the fate of myoblasts transplanted into muscles of dystrophic mice, finding that the majority of the grafted cells quickly die and only a minority are responsible for new muscle formation. This minority is behaviorally distinct, slowly dividing in tissue culture, but rapidly proliferative after grafting, suggesting a subpopulation with stem cell–like characteristics.

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