scholarly journals Cellular therapy of coronary heart disease: a summary of state of the art, limitations and prospects. Part One. Introduction, techniques of myocardial cell transplantation, skeletal myoblasts.

Cor et Vasa ◽  
2006 ◽  
Vol 48 (5) ◽  
pp. 186-190
Author(s):  
Martin Pěnička ◽  
Petr Widimský ◽  
Tomasz Siminiak ◽  
Otto Lang ◽  
Karol Čurila ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cell Transplantation ◽  
Cellular Therapy ◽  
State Of The Art ◽  
Myocardial Cell ◽  
Skeletal Myoblasts

scholarly journals Cellular therapy of coronary heart disease: a review of concepts, limitations, prospects. Part Two. Stem cells, prospects of cullular therapy

Cor et Vasa ◽  
2006 ◽  
Vol 48 (6) ◽  
pp. 234-241
Author(s):  
Martin Pěnička ◽  
Petr Widimský ◽  
Tomasz Siminiak ◽  
Otto Lang ◽  
Karol Čurila ◽  
...  
Keyword(s):  
Stem Cells ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Cellular Therapy

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.

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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