Photosensitization Reaction-Induced Electrophysiological Response of Myocardial Cells Dependent on Subcellular Photosensitizer Distribution

2009 ◽  
pp. 229-231
Author(s):  
A. Ito ◽  
H. Matsuo ◽  
T. Suenari ◽  
T. Kimura ◽  
S. Miyoshi ◽  
...  
Keyword(s):  
Myocardial Cells ◽  
Electrophysiological Response

The Ultrastructure of Myocardial Cells in Normal and Cardiac Lethal Mutant Mexican Axolotls, (Ambystoma Mexicanum)

1970 ◽  
Vol 28 ◽  
pp. 62-63
Author(s):  
Larry F. Lemanski ◽  
Eldridge M. Bertke ◽  
J. T. Justus
Keyword(s):  
Fine Structure ◽  
Heart Development ◽  
Osmium Tetroxide ◽  
Picric Acid ◽  
Ambystoma Mexicanum ◽  
Recessive Mutation ◽  
Acid Mixture ◽  
Myocardial Cells ◽  
Lethal Mutant ◽  
Mexican Axolotl

A recessive mutation has been recently described in the Mexican Axolotl, Ambystoma mexicanum; in which the heart forms structurally, but does not contract (Humphrey, 1968. Anat. Rec. 160:475). In this study, the fine structure of myocardial cells from normal (+/+; +/c) and cardiac lethal mutant (c/c) embryos at Harrison's stage 40 was compared. The hearts were fixed in a 0.1 M phosphate buffered formaldehyde-glutaraldehyde-picric acid-styphnic acid mixture and were post fixed in 0.1 M s-collidine buffered 1% osmium tetroxide. A detailed study of heart development in normal and mutant embryos from stages 25-46 will be described elsewhere.

Immunocytochemical localization of desmin and vimentin in chick embryonic myocardial cells

1990 ◽  
Vol 48 (3) ◽  
pp. 448-449
Author(s):  
Yukiko Sugi
Keyword(s):  
Sodium Methoxide ◽  
Intermediate Filament Protein ◽  
Chick Embryos ◽  
Immunocytochemical Localization ◽  
Myocardial Cells ◽  
Immunofluorescence Study ◽  
Immunofluorescent Localization ◽  
Rabbit Igg ◽  
Semithin Sections ◽  
Filament Protein

In cultured skeletal muscle cells of chick, one intermediate filament protein, vimentin, is primarily formed and then synthesis of desmin follows. Coexistence of vimentin and desmin has been immunocytochemically confirmed in chick embryonic skeletal musclecells. Immunofluorescent localization of vimentin and desmin has been described in developing myocardial cells of hamster. However, initial localization of desmin and vimentin in early embryonic heart has not been reported in detail. By quick-freeze deep-etch method a loose network of intermediate filaments was revealed to exist surrounding myofibrils. In this report, immunocytochemical localization of desmin and vimentin is visualized in early stages of chick embryonic my ocardium.Chick embryos, Hamburger-Hamilton (H-H) stage 8 to hatch, and 1 day old postnatal chicks were used in this study. For immunofluorescence study, each embryo was fixed with 4% paraformaldehyde and embedded in Epon 812. De-epoxinized with sodium methoxide, semithin sections were stained with primary antibodies (rabbit anti-desmin antibody and anti-vimentin antibody)and secondary antibody (RITC conjugated goat-anti rabbit IgG).

Allogenic biomaterial - an inducer of autologous stem and committed myocardial cells in ischemic damaged myocardium

2019 ◽  
Vol 17 (1) ◽  
pp. 89-94 ◽  
Author(s):  
E. R. Muldashev ◽  
◽  
A. I. Lebedeva ◽  
S. A. Muslimov ◽  
S. V. Popov ◽  
...  
Keyword(s):  
Myocardial Cells

Paracrine Mechanisms Involved in Mesenchymal Stem Cell Differentiation into Cardiomyocytes

2019 ◽  
Vol 14 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Maryam Farzaneh ◽  
Fatemeh Rahimi ◽  
Masoumeh Alishahi ◽  
Seyed E. Khoshnam
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Dysfunction ◽  
Stem Cell Differentiation ◽  
Myocardial Cells ◽  
Coronary Artery Diseases ◽  
Low Cardiac Output ◽  
Mesenchymal Stem Cell Differentiation ◽  
Proliferation And Differentiation ◽  
The World ◽  
Biochemical Analyses

Cardiovascular disease (CVD) is one of the world-wide healthcare problem that involves the heart or blood vessels. CVD includes myocardial infarction and coronary artery diseases (CAD). Dysfunctional myocardial cells are leading causes of low cardiac output or ventricular dysfunction after cardiac arrest and may contribute to the progression of CVD which could not generate new cardiomyocytes in human adult heart. The mesenchymal stem cells (MSCs) which are present in adult marrow can self-renew and have the capacity of differentiation into multiple types of cells including cardiomyocytes. Recent biochemical analyses greatly revealed that several regulators of MSCs, such as HGF, PDGF, Wnt, and Notch-1 signaling pathways have been shown to be involved in the proliferation and differentiation into cardiomyocytes. Preclinical studies are paving the way for further applications of MSCs in the repair of myocardial infarction. In this study, we discuss and summarize the paracrine mechanisms involved in MSCs differentiation into cardiomyocytes.

ALDH2 Expression In Myocardial Cells Is Increased In Response To Hypoxia Followed By Reoxygenation

2014 ◽  
Vol 186 (2) ◽  
pp. 494
Author(s):  
C.T. Holley ◽  
M.E. Lindsey ◽  
E.M. Chappuis ◽  
E.O. McFalls ◽  
R.F. Kelly ◽  
...  
Keyword(s):  
Myocardial Cells

scholarly journals Complement C9 expression is associated with damaged myocardial cells in pediatric sudden death cases of fulminant myocarditis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Akari Takaya Uno ◽  
Masahito Hitosugi ◽  
Mami Nakamura ◽  
Tomoyuki Nakanishi ◽  
Takahiro Mima ◽  
...  
Keyword(s):  
Sudden Death ◽  
Acute Myocarditis ◽  
Lymphocytic Infiltration ◽  
Pericardial Fluid ◽  
Sirtuin 1 ◽  
Fulminant Myocarditis ◽  
Myocardial Cells ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining ◽  
Complement C9

Abstract Background Because disease progression is so fast in sudden death of acute fulminant myocarditis, damage of myocardial cells is not evident in routine hematoxylin and eosin staining. To understand damage to myocardial cells and the mechanism of sudden death, immunohistochemical staining was performed for two forensic autopsy cases. Case presentation The patients were a healthy 5-year-old girl and 8-year-old boy. They suddenly died within 2 days of appearance of flu-like symptoms. An autopsy showed accumulation of yellowish-clear pericardial fluid containing fibrin deposits, fluid blood in the heart, and congestion of visceral organs. Histologically, minor necrosis or degeneration of myocardial cells with mainly lymphocytic infiltration was observed sometimes in tissue sections. Immunohistochemically, positive complement C9 staining and negative sirtuin 1 staining were found. These findings suggested wide damage of myocardial cells, even in regions with no marked changes in myocardial cells with hematoxylin and eosin staining. These areas corresponded to those with strong accumulation of lymphocytes. Conclusions Immunohistochemistry for complement C9 and sirtuin 1 might become a new tool for evaluating damage of myocardial cells of fulminant acute myocarditis.

scholarly journals ELAVL1 is transcriptionally activated by FOXC1 and promotes ferroptosis in myocardial ischemia/reperfusion injury by regulating autophagy

2021 ◽  
Vol 27 (1) ◽  
Author(s):  
Hui-Yong Chen ◽  
Ze-Zhou Xiao ◽  
Xiao Ling ◽  
Rong-Ning Xu ◽  
Peng Zhu ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Beclin 1 ◽  
Myocardial Cells ◽  
Myocardial Ischemia And Reperfusion ◽  
Functional Roles ◽  
Cellular Iron ◽  
Luciferase Activity Assay ◽  
Myocardial Ischemia Reperfusion

Abstract Aims Myocardial ischemia is the most common form of cardiovascular disease and the leading cause of morbidity and mortality. Understanding the mechanisms is very crucial for the development of effective therapy. Therefore, this study aimed to investigate the functional roles and mechanisms by which ELAVL1 regulates myocardial ischemia and reperfusion (I/R) injury. Methods Mouse myocardial I/R model and cultured myocardial cells exposed to hypoxia/reperfusion (H/R) were used in this study. Features of ferroptosis were evidenced by LDH activity, GPx4 activity, cellular iron, ROS, LPO, and GSH levels. The expression levels of autophagy markers (Beclin-1, p62, LC3), ELAVL1 and FOXC1 were measured by qRT-PCR, immunostaining and western blot. RIP assay, biotin-pull down, ChIP and dual luciferase activity assay were employed to examine the interactions of ELAVL1/Beclin-1 mRNA and FOXC1/ELAVL1 promoter. CCK-8 assay was used to examine viability of cells. TTC staining was performed to assess the myocardial I/R injury. Results Myocardial I/R surgery induced ferroptosis and up-regulated ELAVL1 level. Knockdown of ELAVL1 decreased ferroptosis and ameliorated I/R injury. Si-ELAVL1 repressed autophagy and inhibition of autophagy by inhibitor suppressed ferroptosis and I/R injury in myocardial cells. Increase of autophagy could reverse the effects of ELAVL1 knockdown on ferroptosis and I/R injury. ELAVL1 directly bound with and stabilized Beclin-1 mRNA. Furthermore, FOXC1 bound to ELAVL1 promoter region and activated its transcription upon H/R exposure. Conclusion FOXC1 transcriptionally activated ELAVL1 may promote ferroptosis during myocardial I/R by modulating autophagy, leading to myocardial injury. Inhibition of ELAVL1-mediated autophagic ferroptosis would be a new viewpoint in the treatment of myocardial I/R injury.

Anesthetic Effects on Mitochondrial ATP-sensitive K Channel

2001 ◽  
Vol 95 (6) ◽  
pp. 1435-1440 ◽  
Author(s):  
Shinji Kohro ◽  
Quinn H. Hogan ◽  
Yuri Nakae ◽  
Michiaki Yamakage ◽  
Zeljko J. Bosnjak
Keyword(s):  
Fluorescence Microscopy ◽  
Volatile Anesthetics ◽  
Cardioprotective Effect ◽  
K Channel ◽  
Myocardial Cells ◽  
Intravenous Anesthetics ◽  
Inhalational Anesthetics ◽  
Cardioprotective Effects ◽  
Cardiac Preconditioning ◽  
Dose Dependent

Background Volatile anesthetics show an ischemic preconditioning-like cardioprotective effect, whereas intravenous anesthetics have cardioprotective effects for ischemic-reperfusion injury. Although recent evidence suggests that mitochondrial adenosine triphosphate-regulated potassium (mitoK(ATP)) channels are important in cardiac preconditioning, the effect of anesthetics on mitoK(ATP) is unexplored. Therefore, the authors tested the hypothesis that anesthetics act on the mitoK(ATP) channel and mitochondrial flavoprotein oxidation. Methods Myocardial cells were isolated from adult guinea pigs. Endogenous mitochondrial flavoprotein fluorescence, an indicator of mitochondrial flavoprotein oxidation, was monitored with fluorescence microscopy while myocytes were exposed individually for 15 min to isoflurane, sevoflurane, propofol, and pentobarbital. The authors further investigated the effect of 5-hydroxydeanoate, a specific mitoK(ATP) channel antagonist, on isoflurane- and sevoflurane-induced flavoprotein oxidation. Additionally, the effects of propofol and pentobarbital on isoflurane-induced flavoprotein oxidation were measured. Results Isoflurane and sevoflurane induced dose-dependent increases in flavoprotein oxidation (isoflurane: R2 = 0.71, n = 50; sevoflurane: R2 = 0.86, n = 20). The fluorescence increase produced by both isoflurane and sevoflurane was eliminated by 5-hydroxydeanoate. Although propofol and pentobarbital showed no significant effects on flavoprotein oxidation, they both dose-dependently inhibited isoflurane-induced flavoprotein oxidation. Conclusions Inhalational anesthetics induce flavoprotein oxidation through opening of the mitoK(ATP) channel. This may be an important mechanism contributing to anesthetic-induced preconditioning. Cardioprotective effects of intravenous anesthetics may not be dependent on flavoprotein oxidation, but the administration of propofol or pentobarbital may potentially inhibit the cardioprotective effect of inhalational anesthetics.

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