The influence of iron availability on the structural changes of skeletal muscle cells and cardiac muscle cells

2021 ◽  
Vol 8 ◽  
pp. 11-16
Author(s):  
Kamil A. Kobak
Keyword(s):  
Cardiac Muscle ◽  
Cell Morphology ◽  
Structural Changes ◽  
Muscle Cells ◽  
Iron Availability ◽  
Cardiac Muscle Cells ◽  
Skeletal Myocytes ◽  
Hypoxic Conditions ◽  
Iron Deficient

In the presented study, the influence iron availability on the cell morphology and structure was examined in skeletal myocytes cultured under normoxic and hypoxic conditions. The study showed that iron deficiency in vitro (especially in combination with hypoxia) has a detrimental effect on skeletal myocytes. Cellular disfunction was manifested by atrophic changes in cell morphology, structural remodeling of cells and increased expression of muscle atrophy markers. Interestingly, increased iron availability appeared to have some protective properties in the context of aforementioned changes. Moreover, based on clinical data and recent transgenic models, structural and functional abnormalities in iron-deficient cardiac muscle were described and the potential pathomechanisms behind them have been discussed.

Microwave Radiation Effects on Cardiac Muscle Cells in Vitro

1981 ◽  
Vol 86 (2) ◽  
pp. 358 ◽  
Author(s):  
M. J. Galvin ◽  
C. A. Hall ◽  
D. I. McRee
Keyword(s):  
Cardiac Muscle ◽  
Microwave Radiation ◽  
Radiation Effects ◽  
Muscle Cells ◽  
Cardiac Muscle Cells

Effects of carbon monoxide on cardiac muscle cells in culture

1988 ◽  
Vol 255 (3) ◽  
pp. C291-C296 ◽  
Author(s):  
A. C. Nag ◽  
K. C. Chen ◽  
M. Cheng
Keyword(s):  
Growth Rate ◽  
Cardiac Muscle ◽  
Structural Organization ◽  
Optimal Growth ◽  
Muscle Cells ◽  
Cellular Growth ◽  
Cardiac Muscle Cells ◽  
Cells In Culture ◽  
Significant Difference

Embryonic rat cardiac muscle cells grown in the presence of various tensions of CO (5-95%) without the presence of O2 survived and exhibited reduced cell growth, which was concentration dependent. When cardiac muscle cells were grown in the presence of a mixture of CO (10-20%) and O2 (10-20%), the growth rate of these cells was comparable to that of the control cells. Cardiac myocytes continued to beat when exposed to varying tensions of CO, except in the case of 95% CO. The cells exposed to different concentrations of CO contained fewer myofibrils of different stages of differentiation compared with the control and the culture exposed to a mixture of 20% O2 and 20% CO, with cells that contained abundant, highly differentiated myofibrils. There was no significant difference in the structural organization of mitochondria between the control and the surviving experimental cells. It is evident from the present studies that O2 is required for the optimum in vitro cellular growth of cardiac muscle. Furthermore, CO in combination with O2 at a concentration of 10 or 20% can produce optimal growth of cardiac muscle cells in culture.

scholarly journals Mitosis in Beating Cardiac Muscle Cells from Newt Embryos In Vitro

1981 ◽  
Vol 23 (3) ◽  
pp. 237-244 ◽  
Author(s):  
HIROYUKI KANEKO ◽  
ABE SHIN-ICHI ◽  
SHIZUO ITO
Keyword(s):  
Cardiac Muscle ◽  
Muscle Cells ◽  
Cardiac Muscle Cells

DNA synthesis and mitosis in adult amphibian cardiac muscle cells in vitro

Science ◽  
1979 ◽  
Vol 205 (4412) ◽  
pp. 1281-1282 ◽  
Author(s):  
A. Nag ◽  
C. Healy ◽  
M Cheng
Keyword(s):  
Dna Synthesis ◽  
Cardiac Muscle ◽  
Muscle Cells ◽  
Cardiac Muscle Cells

scholarly journals Human Relaxin-2 (Serelaxin) Attenuates Oxidative Stress in Cardiac Muscle Cells Exposed In Vitro to Hypoxia–Reoxygenation. Evidence for the Involvement of Reduced Glutathione Up-Regulation

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 774
Author(s):  
Silvia Nistri ◽  
Claudia Fiorillo ◽  
Matteo Becatti ◽  
Daniele Bani
Keyword(s):  
Oxidative Stress ◽  
Cardiac Muscle ◽  
Reduced Glutathione ◽  
Cell Damage ◽  
Antioxidant Properties ◽  
Muscle Cells ◽  
Protective Effects ◽  
Cardiac Muscle Cells ◽  
Relaxin 2

Serelaxin (RLX) designates the pharmaceutical form of the human natural hormone relaxin-2 that has been shown to markedly reduce tissue and cell damage induced by hypoxia and reoxygenation (HR). The evidence that RLX exerts similar protective effects on different organs and cells at relatively low, nanomolar concentrations suggests that it specifically targets a common pathogenic mechanism of HR-induced damage, namely oxidative stress. In this study we offer experimental evidence that RLX (17 nmol L-1), added to the medium of HR-exposed H9c2 rat cardiac muscle cells, significantly reduces cell oxidative damage, mitochondrial dysfunction and apoptosis. These effects appear to rely on the up-regulation of the cellular availability of reduced glutathione (GSH), a ubiquitous endogenous antioxidant metabolite. Conversely, superoxide dismutase activity was not influenced by RLX, which, however, was not endowed with chemical antioxidant properties. Taken together, these findings verify the major pharmacological role of RLX in the protection against HR-induced oxidative stress, and shed first light on its mechanisms of action.

Translation of heart preproenkephalin mRNA and secretion of enkephalin peptides from cultured cardiac myocytes

1992 ◽  
Vol 263 (5) ◽  
pp. H1560-H1566 ◽  
Author(s):  
J. P. Springhorn ◽  
W. C. Claycomb
Keyword(s):  
Cardiac Muscle ◽  
Muscle Cells ◽  
Neonatal Rat ◽  
Ribonuclease Protection Assay ◽  
Cardiac Muscle Cells ◽  
Adult Rat ◽  
Rabbit Reticulocyte Lysate System ◽  
Ribonuclease Protection ◽  
Carboxy Terminal

Rat ventricular cardiac muscle has previously been shown to contain exceptionally high levels of preproenkephalin mRNA (ppEnk mRNA). We have recently determined that the level of ppEnk mRNA is developmentally and hormonally regulated in rat ventricular cardiac muscle tissue and in cultured myocytes (J. P. Springhorn and W. C. Claycomb. Biochem. J. 258: 73-77, 1989). We demonstrate in the current study that heart ppEnk mRNA is structurally identical at the 5' end to brain ppEnk mRNA using a ribonuclease protection assay and that heart ppEnk mRNA can be translated in vitro using a rabbit reticulocyte lysate system. In vitro synthesized preproenkephalin peptides were immunoprecipitated with a polyclonal antibody directed to the carboxy-terminal seven amino acids of preproenkephalin. We have also established by radioimmunoassay that enkephalin-containing peptides are secreted from cultured neonatal and adult rat ventricular cardiac muscle cells. This secretion is linear with respect to time and can be stimulated by phorbol 12-myristate 13-acetate (PMA) and adenosine 3',5'-cyclic monophosphate (cAMP). It was determined by column chromatography that cAMP induced neonatal rat ventricular cardiac muscle cells to secrete Met5-enkephalin-Arg6-Phe7, whereas PMA plus 3-isobutyl-1-methylxanthine induced adult rat ventricular cardiac muscle cells to secrete Met5-enkephalin. These studies establish that ventricular heart muscle ppEnk mRNA can be translated and that enkephalin peptides are secreted from ventricular cardiac muscle cells.

Differentiation and integrity of cardiac muscle cells are impaired in the absence of beta 1 integrin

1996 ◽  
Vol 109 (13) ◽  
pp. 2989-2999 ◽  
Author(s):  
R. Fassler ◽  
J. Rohwedel ◽  
V. Maltsev ◽  
W. Bloch ◽  
S. Lentini ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Cardiac Muscle ◽  
Action Potentials ◽  
Embryonic Stem ◽  
Muscle Cells ◽  
Cellular Interactions ◽  
Cardiac Muscle Cells ◽  
Beta 1 Integrin

Cellular interactions with substrata of the microenvironment are one of the major mechanisms for differentiation and morphogenesis. Many of these interactions are mediated via the beta 1 integrin subfamily of cell surface receptors, which are believed to transduce signals upon cell adhesion. We have used beta 1 integrin-deficient embryonic stem cells to test their ability to differentiate into cardiac muscle cells. We show here by several approaches that beta 1 integrin is important for normal cardiogenesis. First, the in vitro differentiation of beta 1 integrin-deficient embryonic stem cells into cardiac muscle cells is retarded. This is demonstrated by the delayed expression of cardiac muscle-specific genes and action potentials. Second, the specification of cardiac precursor cells into pacemaker-, atrial- and ventricular-like cells is significantly impaired in beta 1 integrin-deficient cells. The occurrence of atrial- and ventricular-like cells is reduced and transient. Only cells exhibiting peacemaker-like action potentials of high frequency and arrhythmias survive. Third, the sarcomeric architecture is incomplete and disarranged in the absence of beta 1 integrin. Fourth, beta 1-deficient embryonic stem cells can contribute to the developing heart in chimaeric mice but many areas with beta 1-null cells contain cell debris. The number of beta 1-null cells decrease from prenatal to postnatal stages and is lost completely in 6-month-old hearts. Thus, we conclude that interactions with the extracellular matrix via beta 1 integrin is necessary for differentiation and the maintenance of a specialized phenotype of cardiac muscle cells.

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