Surface Features of Striated Muscle

1968 ◽  
Vol 3 (4) ◽  
pp. 467-474
Author(s):  
D. G. RAYNS ◽  
F. O. SIMPSON ◽  
W. S. BERTAUD
Keyword(s):  
Striated Muscle ◽  
Myocardial Cell ◽  
Fracture Plane ◽  
Myocardial Cells ◽  
General Survey ◽  
Inner Surface ◽  
Ordered Array ◽  
Capillary Endothelial Cells ◽  
Pinocytotic Vesicles ◽  
T Tubules

A general survey of guinea-pig myocardium was undertaken using the freeze-etch technique. Replicas of myocardial cell membranes were obtained. These showed an ordered array of pits or stumps situated at Z levels. The pits are interpreted as the apertures of the transverse tubules (T-tubules) seen from outside the cell, and the stumps as the remnants of the T-tubules remaining attached to the cell membrane after the cell contents have been removed. Pinocytotic vesicles were also present. T-tubules, mitochondria and myofilaments could be seen in replicas of the interior of myocardial cells. Capillary endothelial cells were seen from various aspects; pinocytotic vesicles were their most prominent feature. The appearances of the cell membrances in the present study suggest that the fracture plane tends to pass along either the outer or the inner surface of the membrane rather than of split the membrane.

scholarly journals The apoptotic effect and the plausible mechanism of microwave radiation on rat myocardial cells

2016 ◽  
Vol 94 (8) ◽  
pp. 849-857
Author(s):  
Wenhe Zhu ◽  
Yan Cui ◽  
Xianmin Feng ◽  
Yan Li ◽  
Wei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular System ◽  
Microwave Radiation ◽  
Structural Damage ◽  
Biological Effects ◽  
Microwave Treatment ◽  
Myocardial Cell ◽  
Integrated System ◽  
Myocardial Cells ◽  
Apoptotic Effect

Microwaves may exert adverse biological effects on the cardiovascular system at the integrated system and cellular levels. However, the mechanism underlying such effects remains poorly understood. Here, we report a previously uncharacterized mechanism through which microwaves damage myocardial cells. Rats were treated with 2450 MHz microwave radiation at 50, 100, 150, or 200 mW/cm2 for 6 min. Microwave treatment significantly enhanced the levels of various enzymes in serum. In addition, it increased the malondialdehyde content while decreasing the levels of antioxidative stress enzymes, activities of enzyme complexes I–IV, and ATP in myocardial tissues. Notably, irradiated myocardial cells exhibited structural damage and underwent apoptosis. Furthermore, Western blot analysis revealed significant changes in expression levels of proteins involved in oxidative stress regulation and apoptotic signaling pathways, indicating that microwave irradiation could induce myocardial cell apoptosis by interfering with oxidative stress and cardiac energy metabolism. Our findings provide useful insights into the mechanism of microwave-induced damage to the cardiovascular system.

scholarly journals Characterization of the sarcoplasmic reticulum proteins in the thermogenic muscles of fish.

1994 ◽  
Vol 127 (5) ◽  
pp. 1275-1287 ◽  
Author(s):  
B A Block ◽  
J O'Brien ◽  
G Meissner
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Direct Evidence ◽  
Striated Muscle ◽  
High Capacity ◽  
Muscle Cells ◽  
Immunoblot Analysis ◽  
Fluorescent Labeling ◽  
T Tubules ◽  
The Brain

Marlins, sailfish, spearfishes, and swordfish have extraocular muscles that are modified into thermogenic organs beneath the brain. The modified muscle cells, called heater cells, lack organized myofibrils and are densely packed with sarcoplasmic reticulum (SR), transverse (T) tubules, and mitochondria. Thermogenesis in the modified extraocular muscle fibers is hypothesized to be associated with increased energy turnover due to Ca2+ cycling at the SR. In this study, the proteins associated with sequestering and releasing Ca2+ from the SR (ryanodine receptor, Ca2+ ATPase, calsequestrin) of striated muscle cells were characterized in the heater SR using immunoblot and immunofluorescent techniques. Immunoblot analysis with a monoclonal antibody that recognizes both isoforms of nonmammalian RYRs indicates that the fish heater cells express only the alpha RYR isoform. The calcium dependency of [3H]ryanodine binding to the RYR isoform expressed in heater indicates functional identity with the non-mammalian alpha RYR isoform. Fluorescent labeling demonstrates that the RYR is localized in an anastomosing network throughout the heater cell cytoplasm. Measurements of oxalate supported 45Ca2+ uptake, Ca2+ ATPase activity, and [32P]phosphoenzyme formation demonstrate that the SR contains a high capacity for Ca2+ uptake via an ATP dependent enzyme. Immunoblot analysis of calsequestrin revealed a significant amount of the Ca2+ binding protein in the heater cell SR. The present study provides the first direct evidence that the heater SR system contains the proteins necessary for Ca2+ release, re-uptake and sequestration, thus supporting the hypothesis that thermogenesis in the modified muscle cells is achieved via an ATP-dependent cycling of Ca2+ between the SR and cytosolic compartments.

Investigate the Effect of miR-22 on the Apoptosis of Coronary Heart Disease Cells Through the Wnt-1 Pathway Based on Nano-Silica-Induced Rat Models

2021 ◽  
Vol 21 (2) ◽  
pp. 1338-1344
Author(s):  
Fangjing Wei ◽  
Baojun Ren ◽  
Wei Han ◽  
Hong Guan ◽  
Guoqiang Jing ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Myocardial Cell ◽  
Control Group ◽  
Myocardial Cells ◽  
Nano Silica ◽  
Rat Cardiomyocytes

In this paper, by examining the toxicity of nano-silica to coronary heart disease cells, we explored the apoptosis of rat myocardial cells induced by nano-silica, and explored the effect of apoptosis on cells during the process of myocardial cytotoxicity induced by nano-silica. This article selects rat cardiomyocytes as the research object and conducts a group control experiment. A control group is set up with cells that are not stained with nano-silica. Different concentrations of nanosilica suspensions are applied to rat cells and detected by CCK-8 method. Cell survival rate after exposure to different concentrations of cells is used to determine the most stable exposure time and concentration. We used flow cytometry to detect intracellular reactive oxygen species and apoptotic rates, and used Western Blot to detect the expression of proteins that affect apoptosis. Finally, we investigated the effect of the Wnt signaling pathway on coronary heart disease. The Wnt signaling pathway regulates the development of the heart and blood vessels. In the treatment of cardiovascular disease, this pathway will be activated again to play a regulatory role. We conclude that nano-silica can induce cytotoxicity in rat myocardial cells through the Wnt-1 pathway, and nanosilica can induce myocardial cell apoptosis through the Wnt-1 pathway.

Anti-apoptotic effects of myocardin-related transcription factor-A on rat cardiomyocytes following hypoxia-induced injury

2016 ◽  
Vol 94 (4) ◽  
pp. 379-387 ◽  
Author(s):  
Ze Zhong ◽  
Jia-qing Hu ◽  
Xin-dong Wu ◽  
Yong Sun ◽  
Jun Jiang
Keyword(s):  
Transcription Factor ◽  
Ischemia Reperfusion ◽  
Myocardial Cell ◽  
Myocardial Cells ◽  
Wild Type ◽  
Cardiac Damage ◽  
Rat Cardiomyocytes ◽  
Related Transcription Factor ◽  
Myocardial Ischemia Reperfusion ◽  
Apoptotic Effects

Myocardin-related transcription factor-A (MRTF-A) can transduce both biomechanical and humoral signals, which can positively modulate cardiac damage induced by acute myocardial infarction. However, the molecular mechanism that underlies the contribution that MRTF-A provides to the myocardium is not completely understood. The objective of this study was to investigate the effects of MRTF-A on myocardium apoptosis and its mechanisms. Our experiment results showed that MRTF-A expression increased and Bcl-2 expression reduced during myocardial ischemia–reperfusion in rat. Meanwhile, primary cardiomyocytes were pretreated with wild-type MRTF-A or siRNA of MRTF-A before exposure to hypoxia. We found that overexpression of MRTF-A in myocardial cells inhibited apoptosis and the release of cytochrome c. MRTF-A enhanced Bcl-2, which contributes to MRTF-A interaction with Bcl-2 in the nuclei of cardiomyocytes. MRTF-A upregulation expression of Bcl-2 in cardiomyocytes induced by hypoxia was inhibited by PD98059, an ERK1/2 inhibitor. In conclusions, MRTF-A improved myocardial cell survival in a cardiomyocyte model of hypoxia-induced injury; this effect was correlated with the upregulation of anti-apoptotic gene Bcl-2 through the activation of ERK1/2.

scholarly journals Role of Thrombospondin-1 in Sepsis-Induced Myocardial Injury

2021 ◽  
Author(s):  
YUN XIE ◽  
JIAXIANG ZHANG ◽  
WEI JIN ◽  
RUI TIAN ◽  
Ruilan Wang
Keyword(s):  
Mrna Expression ◽  
Real Time ◽  
Quantitative Pcr ◽  
Myocardial Injury ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Expression Level ◽  
Myocardial Cells ◽  
Thrombospondin 1 ◽  
Myocardial Cell Injury

Abstract Objective: Sepsis often causes myocardial injury with a high mortality. We wanted to investigate the effects of thrombospondin-1 (THBS1) expression on myocardial cell injury, oxidative stress and apoptosis in sepsis.Methods: The expression of THBS1 mRNA in LPS-induced mouse primary cardiomyocytes was detected by real-time fluorescence quantitative PCR. We constructed a eukaryotic siRNA expression vector and used liposome transfection to knockdown THBS1 mRNA expression in myocardial cells. We detected the THBS1 mRNA expression level using real-time fluorescent quantitative PCR. Four groups were used: control, LPS, THBS1 siRNA, and LPS + THBS1 siRNA. ELISA was used to detect cTnI, proBNP, ROS, caspase3 and other indicators of cell damage. At the same time, sepsis mouse models were prepared for H&E, TUNEL and caspase-3 staining to evaluate myocardial cell injury and apoptosis. Clinical samples were collected to analyze the serum THBS1 level and correlate it with the prognosis of patients with myocardial injury of sepsis.Results: The expression level of THBS1 mRNA in myocardial cells induced by LPS was increased, and the serum THBS1 level in patients with myocardial injury in sepsis was also significantly increased. In the THBS1 siRNA group with myocardial injury, the levels of cTnI and proBNP were significantly decreased, the levels of the inflammatory cytokines IL-6 and TNF-α were significantly decreased, ROS were significantly decreased, and caspase3 was significantly decreased, and myocardial cell apoptosis was also reduced in the sepsis mouse model. Conclusion: THBS1 is closely related to the biological behavior of myocardial cells and may be a therapeutic target for myocardial injury in sepsis.

scholarly journals Modelling depolarization delay, sodium currents, and electrical potentials in cardiac transverse tubules

2019 ◽  
Author(s):  
Sarah H. Vermij ◽  
Hugues Abriel ◽  
Jan P. Kucera
Keyword(s):  
Striated Muscle ◽  
Sodium Current ◽  
Cardiac Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Tubular Membrane ◽  
Electrical Potentials ◽  
Tubular Lumen ◽  
T Tubules ◽  
Extracellular Potentials

ABSTRACTT-tubules are invaginations of the lateral membrane of striated muscle cells that provide a large surface for ion channels and signaling proteins, thereby supporting excitation-contraction coupling. T-tubules are often remodeled in heart failure. To better understand the electrical behavior of T-tubules of cardiac cells in health and disease, this study addresses two largely unanswered questions regarding their electrical properties: (1) the delay of T-tubular membrane depolarization and (2) the effects of T-tubular sodium current on T-tubular potentials.Here, we present an elementary computational model to determine the delay in depolarization of deep T-tubular membrane segments as the narrow T-tubular lumen provides resistance against the extracellular current. We compare healthy tubules to tubules with constrictions and diseased tubules from mouse and human, and conclude that constrictions greatly delay T-tubular depolarization, and diseased T-tubules depolarize faster than healthy ones due to tubule widening. We moreover model the effect of T-tubular sodium current on intraluminal T-tubular potentials. We observe that extracellular potentials become negative during the sodium current transient (up to −50 mV in constricted T-tubules), which feedbacks on sodium channel function (self-attenuation) in a manner resembling ephaptic effects that have been described for intercalated discs where opposing membranes are very close together.These results show that (1) the excitation-contraction coupling defects seen in diseased cells cannot be explained by T-tubular remodeling alone; and (2) the sodium current may modulate intraluminal potentials. Such extracellular potentials might also affect excitation-contraction coupling.

scholarly journals Astragaloside IV Reduces OxLDL-Induced BNP Overexpression by Regulating HDAC

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Wenting Zhang ◽  
Xin Wang ◽  
Jing Li ◽  
Mingyuan Xu ◽  
Xiaolu Ren ◽  
...  
Keyword(s):  
Treatment Group ◽  
Immunosorbent Assay ◽  
Protein Level ◽  
Cell Injury ◽  
Myocardial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Myocardial Cells ◽  
Astragaloside Iv ◽  
Hdac Activity ◽  
Myocardial Cell Injury

Effective drug intervention is the most important method to improve the prognosis, improve the quality of life, and prolong the life of patients with heart failure. This study aimed to explore the protective effect of astragaloside IV on myocardial cell injury induced by oxidized low-density lipoprotein (OxLDL) and its regulatory mechanism on the increase of brain natriuretic peptide (BNP) caused by myocardial cell injury. The model of myocardial cell injury, protection, and histone deacetylase (HDAC) inhibition in HL-1 mice was established by OxLDL treatment, astragaloside IV intervention, and UF010 coincubation. The effects of OxLDL and astragaloside IV on apoptosis were detected by flow cytometry. The expression level of BNP mRNA and protein in cells was investigated by real-time fluorescence quantification, western blot, and enzyme-linked immunosorbent assay. HDAC activity in nucleus was calibrated by fluorescence absorption intensity. Enzyme-linked immunosorbent assay (ELISA) was applied to test eNOS level in myocardial cells. OxLDL significantly promoted apoptosis, upregulated BNP mRNA, increased BNP protein level inside and outside cells, and decreased eNOS level. Compared with OxLDL treatment group, apoptosis decreased, BNP mRNA expression level decreased, BNP protein concentration decreased, and eNOS level increased significantly combined with low and high concentration astragaloside IV treatment group. HDAC activity significantly increased in OxLDL treatment group and significantly decreased after combined incubation with low and high concentrations of astragaloside IV. Inhibition of HDAC significantly increased eNOS level and decreased BNP protein level. In conclusion, astragaloside IV can reverse the low level of eNOS caused by OxLDL by regulating HDAC activity to protect myocardial cells from oxide damage, which is manifested by the decrease of BNP concentration.

Pores in the Plasma Membranes of Myocardial Cells

1967 ◽  
Vol 25 ◽  
pp. 198-199
Author(s):  
Glenwood P. Epling
Keyword(s):  
Electron Microscopy ◽  
Plasma Membranes ◽  
Polyester Resin ◽  
Uranyl Acetate ◽  
Lead Citrate ◽  
Myocardial Cells ◽  
Pinocytotic Vesicles ◽  
Sarcotubular System ◽  
The Right ◽  
Copper Mesh

Heart muscle samples were collected from the right ventricles of twelve mature cattle and twelve pigs at slaughter and immediately prepared for electron microscopy by immersion in three different fixatives: 40% OsO4 dissolved in CCl4, 1.5% OsO4 in S collidine buffer, and in 2.5%. glutaraldehyde followed by 1.5%, OsO4. Some tissue from each animal was processed in each fixative and was embedded in either an epoxy resin or in a polyester resin. Sections were cut at 300 to 600 Å in thickness on a thermally advancing microtome, using glass and diamond knives, and were mounted on copper mesh grids. Uranyl acetate and lead citrate stains were used. Tissues were examined in an RCA, EMU-3F electron microscope.In both the cattle and pigs, some heart samples contained myocardial cells with plasma membranes which invaginated into the cells to form tubular appearing channels. These channels occurred in addition to the transverse sarcotubular system, and in addition to the pinocytotic vesicles. The basement membrane which surrounds myocardial cells did not extend into the invaginations, but bridged over their external apertures.

A conserved 28-base-pair element (HF-1) in the rat cardiac myosin light-chain-2 gene confers cardiac-specific and alpha-adrenergic-inducible expression in cultured neonatal rat myocardial cells

1991 ◽  
Vol 11 (4) ◽  
pp. 2273-2281
Author(s):  
H Zhu ◽  
A V Garcia ◽  
R S Ross ◽  
S M Evans ◽  
K R Chien
Keyword(s):  
Transient Expression ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Myocardial Cell ◽  
Inducible Expression ◽  
Neonatal Rat ◽  
Cardiac Myosin ◽  
Myocardial Cells ◽  
Myosin Light Chain 2 ◽  
Regulated Expression

To study the transcriptional regulatory mechanisms which mediate cardiac-specific and inducible expression during myocardial cell hypertrophy, we have extensively characterized the rat cardiac myosin light-chain-2 (MLC-2) gene as a model system. The MLC-2 gene encodes a relatively abundant contractile protein in slow skeletal and cardiac muscle and is upregulated during in vivo cardiac hypertrophy and alpha-adrenergic-mediated hypertrophy of neonatal rat myocardial cells. In transient expression assays employing a series of MLC-2-luciferase constructs, recent studies have identified a 250-bp fragment which is sufficient for both cardiac-specific and alpha-adrenergic-inducible expression. Within this 250-bp fragment lie three regions (HF-1, HF-2, and HF-3), each greater than 10 bp in length, which are conserved between the chicken and rat cardiac MLC-2 genes, suggesting their potential role in the regulated expression of this contractile protein gene. As assessed by substitution mutations within each of the conserved regions, the present study demonstrates that HF-1 and HF-2 are important in both cardiac-specific and inducible expression, while HF-3 has no detectable role in the regulated expression of the MLC-2 gene in transient expression assays. HF-1 sequences confer both cardiac-specific and inducible expression to a neutral promoter-luciferase construct but have no significant effect in the skeletal muscle or nonmuscle cell contexts. Thus, these studies have identified a new cardiac-specific regulatory element (HF-1) which plays a role in both cardiac-specific and inducible expression during myocardial cell hypertrophy.

scholarly journals The Protective Effects of miR-21-Mediated Fibroblast Growth Factor 1 in Rats with Coronary Heart Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Bin Zhang ◽  
Hongguang Liu ◽  
Guoping Yang ◽  
Yongmei Wang ◽  
Yan Wang
Keyword(s):  
Blood Pressure ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Growth Factor ◽  
Myocardial Ischemia ◽  
Fibroblast Growth Factor ◽  
Myocardial Cell ◽  
Protective Effects ◽  
Fibroblast Growth ◽  
Myocardial Cells

Aim. The study is to verify the protective effects of miR-21-mediated fibroblast growth factor 1 (FGF1) against myocardial ischemia in rats with coronary heart disease. Materials and Methods. Sprague-Dawley (SD) rat models of myocardial ischemia/reperfusion (MI/R) injury were constructed, and the expression of miR-21 and FGF1 in them was interfered through ischemic postconditioning. The protective effects of miR-21-mediated FGF1 on myocardium of the model rats were analyzed, and the targeted regulatory relationship between miR-21 and FGF1 was verified through myocardial cell experiments to find the mechanism of miR-21. Results. MiR-21 and FGF1 with increased expression could protect the cardiac function of model rats and improve their diastolic blood pressure (DBP), systolic blood pressure (SBP), heart rate (HR), coronary flow (CF), bax, and bcl-2 levels, but it would also cause further increase of vascular endothelial growth factor (VEGF) and decreased infarct size (INF). In addition, intervention through both miR-21 mimics and recombinant human FGF1 could highlight the above changes. Pearson correlation analysis revealed that the expression of miR-21 was positively correlated with that of FGF1, and both miR-21 and FGF1 were significantly and linearly correlated with DBP, SBP, HR, CF, INF, bax, and bcl-2, but they were not significantly correlated with the VEGF level. The myocardial cell experiment results revealed that upregulation of miR-21 or FGF1 could alleviate apoptosis caused by hypoxia/reoxygenation of myocardial cells, and inhibition of the FGF1 expression could hinder the effect of miR-21 against apoptosis of myocardial cells. Dual luciferase reporter assay revealed that transfection of miR-21-mimics could effectively raise the fluorescence intensity of pmirGLO-FGF1-3 ′ UTR Wt but had no significant effect on that of pmirGLO-FGF1-3 ′ UTR Mut. Conclusion. MiR-21 can specifically mediate the expression of FGF1 to relieve MI/R injury, protect the cardiac function, and resist apoptosis.

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