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.

Z-band cross sections in rigor skeletal muscle have similar detailed structures as in tetanized muscle

1992 ◽  
Vol 50 (1) ◽  
pp. 544-545
Author(s):  
M. A. Goldstein ◽  
J. P. Schroeter ◽  
R. J. Edwards
Keyword(s):  
Skeletal Muscle ◽  
Cross Sections ◽  
Two Dimensional ◽  
Detailed Structure ◽  
Contractile State ◽  
Contour Maps ◽  
False Color ◽  
Grey Scale ◽  
Fourier Filtering ◽  
Enhancement Algorithm

We have previously shown that two structural states of the Z-band in muscle cross-sections are related to the contractile state of the muscle. In skeletal muscle at rest, the z-band is in the small square (ss) form, but tetanized muscle exhibits the basket weave (bw) form. Recently, we have shown that skeletal muscle in rigor also exhibits the bw form and dimensions.We have used two dimensional computer enhancement techniques on digitized electron micrographs to compare the detailed structure of the tetanized and rigor Z-band lattices. Both lattice averaging and Fourier filtering techniques were used, with enhanced images 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, information in the enhanced 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.

Effect of taxol on the interaction of tubulin with myosin filaments

1984 ◽  
Vol 62 (9) ◽  
pp. 878-884 ◽  
Author(s):  
Toshihiro Fujii ◽  
Tatsuo Suzuki ◽  
Akira Hachimori ◽  
Michiyo Fujii ◽  
Yoshiyuki Kondo ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Skeletal Muscle ◽  
Atpase Activity ◽  
Cross Section ◽  
Molar Ratio ◽  
Tubulin Polymerization ◽  
Myosin Filaments ◽  
Thin Section Electron Microscopy ◽  
Section Electron ◽  
Section Electron Microscopy

The interaction between polymerized tubulin from porcine brain and myosin from rabbit skeletal muscle was examined. The addition of myosin to the solution of tubulin polymerized by taxol resulted in a remarkable increase in turbidity within a few minutes at 37 °C, and a dense and stable precipitate was formed. The maximal molar ratio of tubulin bound to myosin was calculated to be about 4, while the value was about 2 when 6S tubulin was used. Both podophyllotoxin and colchicine suppressed the taxol-dependent increase of the binding of tubulin to myosin, but only when they were preincubated with tubulin prior to addition of taxol. 6S tubulin inhibited with aetin-activated Mg2+-ATPase activity of myosin, and polymerized tubulin inhibited the Mg-ATPase more than 6S tubulin. Dense precipitates of tubulin and myosin were observed by thin-section electron microscopy. Microtubules were observed to be entangled in myosin filaments and single microtubules were occasionally surrounded by five myosin filaments in a cross section, similar to actin–myosin arrays in muscle. After incubation of tubulin with myosin, taxol was able to induce tubulin polymerization in the same way as it polymerized microtubules in the absence of myosin.

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 MuRF1/TRIM63, Master Regulator of Muscle Mass

2020 ◽  
Vol 21 (18) ◽  
pp. 6663 ◽  
Author(s):  
Dulce Peris-Moreno ◽  
Daniel Taillandier ◽  
Cécile Polge
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Cardiac Functions ◽  
Important Player ◽  
Cardiac Muscles ◽  
Inhibitory Molecules

The E3 ubiquitin ligase MuRF1/TRIM63 was identified 20 years ago and suspected to play important roles during skeletal muscle atrophy. Since then, numerous studies have been conducted to decipher the roles, molecular mechanisms and regulation of this enzyme. This revealed that MuRF1 is an important player in the skeletal muscle atrophy process occurring during catabolic states, making MuRF1 a prime candidate for pharmacological treatments against muscle wasting. Indeed, muscle wasting is an associated event of several diseases (e.g., cancer, sepsis, diabetes, renal failure, etc.) and negatively impacts the prognosis of patients, which has stimulated the search for MuRF1 inhibitory molecules. However, studies on MuRF1 cardiac functions revealed that MuRF1 is also cardioprotective, revealing a yin and yang role of MuRF1, being detrimental in skeletal muscle and beneficial in the heart. This review discusses data obtained on MuRF1, both in skeletal and cardiac muscles, over the past 20 years, regarding the structure, the regulation, the location and the different functions identified, and the first inhibitors reported, and aim to draw the picture of what is known about MuRF1. The review also discusses important MuRF1 characteristics to consider for the design of future drugs to maintain skeletal muscle mass in patients with different pathologies.

Studies on Adenylate Cyclase – Cyclic AMP System of the Myopathic Hamster (UM-X7.1) Skeletal and Cardiac Muscles

1975 ◽  
Vol 53 (10) ◽  
pp. 1122-1127 ◽  
Author(s):  
J. A. C. Harrow ◽  
J. N. Singh ◽  
G. Jasmin ◽  
N. S. Dhalla
Keyword(s):  
Skeletal Muscle ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Skeletal Muscles ◽  
Normal Values ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Amp System ◽  
Cardiac Muscles ◽  
Muscle Homogenate

Cyclic AMP content, adenylate cyclase (EC 4.6.1.1) activity and phosphodiesterase I (EC 3.1.4.1) activity of the hind leg skeletal muscle and cardiac muscle in 60- and 150-day-old normal and myopathic (UM-X7.1) hamsters were examined. In 60-day-old myopathic animals, cardiac cyclic AMP levels were higher and phosphodiesterase I activity was lower, without any changes in the basal adenylate cyclase activity, whereas in 150-day-old myopathic hamsters, cardiac cyclic AMP and basal adenylate cyclase activity were lower, without any changes in the homogenate phosphodiesterase I activity. On the other hand, basal adenylate cyclase and phosphodiesterase I activities in the skeletal muscle homogenate from 60- and 150-day-old myopathic animals were not different from the normal values but the skeletal muscle cyclic AMP levels were significantly less in 60-day-old myopathic hamsters only. The plasma cyclic AMP levels in 60-day-old myopathic hamsters, unlike 150-day-old myopathic animals, were higher than the normal. Although these results reveal differences in myopathic cardiac and skeletal muscles, it is concluded that changes in adenylate cyclase – cyclic AMP system in myopathy are dependent upon the degree of disease.

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.

Real-Space Analysis

2021 ◽  
pp. 223-254
Author(s):  
Andreas Michels
Keyword(s):  
Experimental Data ◽  
Correlation Function ◽  
Cross Section ◽  
Correlation Length ◽  
Permanent Magnets ◽  
Real Space ◽  
Space Analysis ◽  
The Subject ◽  
Cobalt And Nickel

Spin-misalignment correlations in real space are the subject of this chapter. The correlation function and correlation length of the spin-misalignment SANS cross section are introduced, their properties are discussed within the context of micromagnetic theory, and selected experimental data on Nd-Fe-B-based permanent magnets and nanocrystalline elemental soft (Cobalt and Nickel) and hard (Gadolinium and Terbium) magnets are reviewed.

Evolutionary aspects of a new MyoD gene in amphioxus (Branchiostoma belcheri) and its promoter specificity in skeletal and cardiac muscles

Biologia ◽  
2014 ◽  
Vol 69 (9) ◽  
Author(s):  
Xungang Tan ◽  
Pei Zhang ◽  
Shao Du
Keyword(s):  
Skeletal Muscle ◽  
Transcription Factors ◽  
Zebrafish Embryos ◽  
Evolutionary Analysis ◽  
Gene Duplications ◽  
Gfp Expression ◽  
Specific Expression ◽  
Branchiostoma Belcheri ◽  
Cardiac Muscles ◽  
Myod Gene

AbstractVertebrate MyoD family of transcription factors contains four members including MyoD, Myf5, Myogenin and MRF4. These myogenic regulatory factors (MRFs) play key roles in regulating skeletal muscle development and growth. Evolutionary analysis suggests that the four vertebrate MRF genes were derived by gene duplications from a single ancestral gene during chordate evolution. Better understanding of the structure and regulation of MyoD expression in amphioxus Branchiostoma belcheri may provide insight into the evolutionary history of myogenic gene duplications because of the unique position of amphioxus in evolution. We report here that isolation and characterization of a new MyoD gene, AmphiMyoD, in B. belcheri. Sequence analysis revealed that the AmphiMyoD is more closely related to myogenic transcription factors in invertebrates and vertebrates compared with the previously identified three MyoD like genes in amphioxus, suggesting that the AmphiMyoD might be the closest relative of the ancestral myogenic gene. To determine if the AmphiMyoD gene promoter controls muscle-specific expression, the AmphiMyoD promoter was linked with the green fluorescence protein (GFP) reporter and the construct was microinjected into zebrafish embryos for transient expression assay. AmphiMyoD promoter directed skeletal muscle-specific GFP expression in zebrafish embryos. In addition, it also drove GFP expression in cardiac muscles of the injected embryos, but not in other non-muscle tissues. These data demonstrated that the AmphiMyoD promoter contained regulatory elements for skeletal and cardiac muscle-specific expression. Moreover, the regulatory element(s) could function across species.

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