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.

scholarly journals Association of Fibroblast Growth Factor 23 With Risk of Incident Coronary Heart Disease in Community-Living Adults

2018 ◽  
Vol 3 (4) ◽  
pp. 318 ◽  
Author(s):  
Bhupesh Panwar ◽  
Suzanne E. Judd ◽  
Virginia G. Wadley ◽  
Nancy S. Jenny ◽  
Virginia J. Howard ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Community Living ◽  
Fibroblast Growth ◽  
Incident Coronary Heart Disease

scholarly journals Protective Effects of Moderate Ca Supplementation against Cd-Induced Bone Damage under Different Population-Relevant Doses in Young Female Rats

Nutrients ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 849 ◽  
Author(s):  
Huang ◽  
Liu ◽  
Zhao ◽  
Fu ◽  
Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Bone Formation ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Young Female ◽  
Female Rats ◽  
Bone Biomechanics ◽  
Protective Effects ◽  
Fibroblast Growth ◽  
Bone Damage

Estimation of the skeleton-protective effects of Ca in Cd-induced bone damage is helpful in the assessment of Cd health risk. The aim of this study was to identify whether Ca supplementation during exposure to different population-relevant doses of Cd can prevent Cd-induced bone damage under the tolerable upper intake level of Ca supplementation. Young female Sprague-Dawley rats were given different population-relevant doses of Cd (1, 5, and 50 mg Cd/kg diet) and Ca supplementation (0.4% Ca supplementation) intervention. Ca supplementation significantly decreased Cd-induced bone microstructure damage, increased bone biomechanics (p < 0.05), serum bone formation marker level (p < 0.05) and expression of osteogenic gene markers exposure to the 5 and 50 mg Cd/kg diets. However, it had no impact on these indicators under the 1 mg Cd/kg diets, with the exception of expression of osteogenic marker genes. Ca supplementation significantly decreased serum Klotho level (p < 0.05), and fibroblast growth factor 23/Klotho-associated gene expression in the kidney and bone showed significant changes. In conclusion, Ca supplementation has a positive effect on bone formation and bone quality against the damaging impact of Cd, especially with exposure to the 5 mg and 50 mg Cd/kg diet, which may be related to its impact on the fibroblast growth factor 23/Klotho axis.

Fibroblast Growth Factor-2 Mediates Angiotensin Ii-Induced Cardiac Hypertrophy in Renovascular Hypertension

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 683-683
Author(s):  
Corinne Pellieux ◽  
Alessandro Foletti ◽  
Thercse Sauthier ◽  
Aubert Jean-Francois ◽  
Beermann Friedrich ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Fibroblast Growth Factor ◽  
Renovascular Hypertension ◽  
Intracellular Signaling ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Jnk Activation

29 In renovascular hypertension, angiotensin II leads to an elevation of blood pressure and to cardiac hypertrophy. The fibroblast growth factor-2 (FGF-2) has been implicated in cardiomyocyte growth. Therefore, we investigated whether FGF-2 could control the development of angiotensin II-induced cardiac hypertrophy. Mice deficient for the expression of FGF-2 were created, and the role of FGF-2 was investigated in the two kidney-one clip (2K1C) model of renin-dependent hypertension. The activation of the MAPK pathways were shown to be crucial in the intracellular signaling leading to cardiac hypertrophy. Therefore, we followed also the cardiac activation of JNK, ERK and the p38 kinase in these animals. Both wild-type and FGF-2 deficient (FGF-2 -/-) mice showed similar elevation of blood pressure in the 2K1C model. Interestingly, 2K1C FGF-2 -/- mice developed markedly reduced hypertrophy as compared to wild-types. Moreover, in 2K1C wild-types, cardiac hypertrophy developed in association with a concomitant stimulation of JNK, ERK and p38. In contrast, JNK activation was strongly decreased in hypertensive mice deficient for FGF-2, while p38 and ERK were less affected. These data suggest that FGF-2 is important in mediating angiotensin II-induced cardiac hypertrophy in renovascular hypertension via autocrine/paracrine mechanisms.

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.

Serum basic fibroblast growth factor levels in patients with ischemic heart disease

1997 ◽  
Vol 59 (2) ◽  
pp. 133-138 ◽  
Author(s):  
David Hasdai ◽  
Vivian Barak ◽  
Eyal Leibovitz ◽  
Itzhak Herz ◽  
Samuel Sclarovsky ◽  
...  
Keyword(s):  
Heart Disease ◽  
Growth Factor ◽  
Ischemic Heart Disease ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Ischemic Heart ◽  
Fibroblast Growth
Sign in / Sign up

Export Citation Format

Share Document