Effect of long-term cyclic mechanical load on protein synthesis and morphological changes in cultured Myocardial cells from neonatal rat

1994 ◽  
Vol 8 (2) ◽  
pp. 251-262 ◽  
Author(s):  
Yuji Kira ◽  
Takashi Nakaoka ◽  
Etsuo Hashimoto ◽  
Fujiko Okabe ◽  
Shigetaka Asano ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Mechanical Load ◽  
Morphological Changes ◽  
Neonatal Rat ◽  
Myocardial Cells ◽  
Cultured Myocardial Cells ◽  
Cyclic Mechanical Load

Long-term hypoxia exposure enhanced IGFBP-3 protein synthesis and secretion resulting in cell apoptosis in H9c2 myocardial cells

2015 ◽  
Vol 33 (4) ◽  
pp. 275-281 ◽  
Author(s):  
Ruey-Lin Chang ◽  
Jing-Wei Lin ◽  
Dennis Jine-Yuan Hsieh ◽  
Yu-Lan Yeh ◽  
Chia-Yao Shen ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Cell Apoptosis ◽  
Myocardial Cells ◽  
Hypoxia Exposure ◽  
Igfbp 3

Mechanisms of accumulation of arachidonic acid in cultured myocardial cells during ATP depletion

1985 ◽  
Vol 249 (6) ◽  
pp. H1188-H1194 ◽  
Author(s):  
M. D. Gunn ◽  
A. Sen ◽  
A. Chang ◽  
J. T. Willerson ◽  
L. M. Buja ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Atp Depletion ◽  
Neonatal Rat ◽  
Metabolic Inhibitors ◽  
Critical Threshold ◽  
Acid Oxidation ◽  
Arachidonic Acid Release ◽  
Myocardial Cells ◽  
Acid Release ◽  
Cultured Myocardial Cells

Previous studies have suggested that the accumulation of free arachidonic acid may be of major importance in the pathophysiology of myocardial ischemia. The purpose of the present study was to determine if the release of arachidonic acid from myocardial cells was more dependent on the extent of ATP depletion than on the inhibition of fatty acid oxidation. In addition, these studies were designed to determine if arachidonic acid release only occurred when ATP was depleted beyond a critical threshold level. To examine the relationship between arachidonic acid release and ATP depletion, cultured myocardial cells from neonatal rat hearts were labeled with [3H]arachidonate and [14C]palmitate. In response to ATP depletion with various metabolic inhibitors, [3H]arachidonic acid and [14C]palmitic acid were released from phospholipids. Phosphatidylcholine,phosphatidylethanolamine, and phosphatidic acid were the major esterified sources of the arachidonate. The release of both fatty acids was related to the extent of ATP depletion and not whether a glycolytic or respiratory inhibitor was utilized. Various combinations and doses of metabolic inhibitors were used, and experimental conditions that produced a greater than 75% decrease in ATP content were associated with the accumulation of arachidonic acid. These results suggest that an ATP-dependent step may be linked to the accumulation of arachidonic acid during myocardial ATP depletion. It is suggested that myocardial cells may release arachidonic acid directly in response to ATP depletion.

Alpha 1-adrenergic stimulation of rat myocardial cells increases protein synthesis

1986 ◽  
Vol 251 (5) ◽  
pp. H1076-H1084 ◽  
Author(s):  
R. S. Meidell ◽  
A. Sen ◽  
S. A. Henderson ◽  
M. F. Slahetka ◽  
K. R. Chien
Keyword(s):  
Protein Synthesis ◽  
Protein Content ◽  
Primary Cultures ◽  
Neonatal Rat ◽  
Cell Protein ◽  
Heart Cells ◽  
Adrenergic Blockade ◽  
Myocardial Cells ◽  
Adrenergic Stimulation ◽  
Degradation Rates

The effects of adrenergic stimulation on the rates of protein synthesis, degradation, and accumulation were examined in primary cultures of neonatal rat heart cells. Treatment of myocardial cells with norepinephrine increased total cellular protein content and the rate of incorporation of radiolabeled tyrosine into trichloroacetic acid insoluble protein. alpha 1-Adrenergic, but not alpha 2- or beta-adrenergic blockade, inhibited these norepinephrine induced increases. The rate of protein synthesis estimated from the kinetics of equilibrium labeling and from combined equilibrium and pulse labeling was increased by norepinephrine stimulation, whereas protein degradation estimated by release of previously incorporated radiolabeled tyrosine or in pulse-chase experiments was unaffected. To determine whether alpha 1-adrenergic stimulation produced similar effects on the turnover of myofibrillar proteins, rates of synthesis and degradation were estimated for a myofibrillar-enriched protein fraction and for myosin heavy chain and actin. Norepinephrine treatment produced increases in the synthesis of myofibrillar protein without significantly altering degradation rates. These experiments suggest that alpha 1-adrenergic stimulation increases myocardial cell protein content by accelerating protein synthesis.

scholarly journals Effect of verapamil and of extracellular Ca and Na on contraction frequency of cultured heart cells.

1976 ◽  
Vol 68 (5) ◽  
pp. 537-549 ◽  
Author(s):  
D McCall
Keyword(s):  
Petri Dish ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Myocardial Cells ◽  
Contraction Frequency ◽  
Close Relationship ◽  
Show Evidence ◽  
Beating Rate ◽  
Cultured Heart Cells ◽  
Cultured Myocardial Cells

Monolayer cultures of myocardial cells were prepared by trypsin dispersion of neonatal rat ventricles. The cells were cultured for 4-5 days by which time a synchronously contracting monolayer of some 1.0 x 10(6) cells per 6-cm diam petri dish had formed. The contraction frequency and Na influx of the cells were unaffected by tetrodotoxin (2 x 10(-5) mg/ml) but both were markedly reduced by the addition of verapamil (10(-9) M to 10(-5) M). The effect of verapamil on both parameters occurred very rapidly. Although unresponsive to change in [Ca]0 between 0.3 mM and 3.0 mM, the contraction frequency of the cells declined rapidly as the [Ca]0 was reduced below 0.3 mM. On the other hand the beating rate of the cells was linearly related to [Na]0 below 40 mM the cells ceased to contract. It is therefore apparent that both [Ca]0 and [Na]0 contribute to the maintenance of the contraction frequency of cultured myocardial cells, but the latter is by far the more important. There also appeared to be, under all conditions, a close relationship between verapamilsensitive Na influx and contraction frequency. For the greater part this relationship was linear although at higher Na influx values it appeared to show evidence of saturation.

Comparative assessment of morphological mechanisms of maintaining structural liver homeostasis in the dynamics of exposure to coal-rock dust and sodium fluoride on the body

2020 ◽  
pp. 189-194
Author(s):  
M. S. Bugaeva ◽  
O. I. Bondarev ◽  
N. N. Mikhailova ◽  
L. G. Gorokhova
Keyword(s):  
Sodium Fluoride ◽  
Morphological Changes ◽  
The Body ◽  
System Level ◽  
Production Factor ◽  
Coal Rock ◽  
The Impact ◽  
Structural Homeostasis ◽  
Rock Dust

Introduction. The impact on the body of such factors of the production environment as coal-rock dust and fluorine compounds leads to certain shift s in strict indicators of homeostasis at the system level. Maintaining the relative constancy of the internal environment of the body is provided by the functional consistency of all organs and systems, the leading of which is the liver. Organ repair plays a crucial role in restoring the structure of genetic material and maintaining normal cell viability. When this mechanism is damaged, the compensatory capabilities of the organ are disrupted, homeostasis is disrupted at the cellular and organizational levels, and the development of the main pathological processes is noted.The aim of the study is to compare the morphological mechanisms of maintaining structural homeostasis of the liver in the dynamics of the impact on the body of coal-rock dust and sodium fluoride.Materials and methods. Experimental studies were conducted on adult white male laboratory rats. Features of morphological mechanisms for maintaining structural homeostasis of the liver in the dynamics of exposure to coal-rock dust and sodium fluoride were studied on experimental models of pneumoconiosis and fluoride intoxication. For histological examination in experimental animals, liver sampling was performed after 1, 3, 6, 9, 12 weeks of the experiment.Results. The specificity of morphological changes in the liver depending on the harmful production factor was revealed. It is shown that chronic exposure to coal-rock dust and sodium fluoride is characterized by the development of similar morphological changes in the liver and its vessels from the predominance of the initial compensatory-adaptive to pronounced violations of the stromal and parenchymal components. Long-term inhalation of coal-rock dust at 1–3 weeks of seeding triggers adaptive mechanisms in the liver in the form of increased functional activity of cells, formation of double-core hepatocytes, activation of immunocompetent cells and endotheliocytes, ensuring the preservation of the parenchyma and the general morphostructure of the organ until the 12th week of the experiment. Exposure to sodium fluoride leads to early disruption of liver compensatory mechanisms and the development of dystrophic changes in the parenchyma with the formation of necrosis foci as early as the 6th week of the experiment.Conclusions. The study of mechanisms for compensating the liver structure in conditions of long-term exposure to coal-rock dust and sodium fluoride, as well as processes that indicate their failure, and the timing of their occurrence, is of theoretical and practical importance for developing recommendations for the timely prevention and correction of pathological conditions developing in employees of the aluminum and coal industry.The authors declare no conflict of interests.

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