scholarly journals Expression and related mechanisms of miR-330-3p and S100B in an animal model of cartilage injury

2021 ◽  
Vol 49 (9) ◽  
pp. 030006052110394
Author(s):  
Wenming Wu ◽  
Dongming Liang
Keyword(s):  
Animal Model ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Intervention Group ◽  
Cartilage Injury ◽  
Cartilage Tissue ◽  
Control Group ◽  
Fibroblast Growth ◽  
Model Group ◽  
Sham Surgery

Objective To investigate the roles of and relationship between microRNA (miR)-330-3p and S100 calcium-binding protein B (S100B) in an animal model of cartilage injury. Methods This study included 30 New Zealand male rabbits randomly divided into three groups: an intervention group, a model group and a sham surgery control group. Modelling was performed in the intervention and model groups, but in the sham surgery group, only the skin was cut. After modelling, the intervention and model groups were injected with the miR-330-3p overexpression vector GV268-miR-330-3p or the control GV268-N-ODN vector, respectively, twice a week for 7 weeks. Results Levels of interleukin-1β and tumour necrosis factor-α in the synovial fluid were significantly higher in the model group than in the intervention and control groups. The level of miR-330-3p in the cartilage tissue was significantly higher in the control group than in the model group but it was significantly lower compared with the intervention group. Levels of S100B, fibroblast growth factor receptor 1 and fibroblast growth factor-2 in the cartilage tissue of rabbits in the model group were significantly higher compared with the control and intervention groups. Conclusion These findings demonstrate that the upregulation of miR-330-3p can inhibit the expression of S100B.

scholarly journals Correlation of Epidermal Fibroblast Growth Factor and Clinical Improvement of Asthma in Children after Zinc Supplementation

2020 ◽  
Vol 6 (3) ◽  
pp. 61
Author(s):  
Retno Asih Setyoningrum ◽  
Anang Endaryanto ◽  
I Dewa Gede Ugrasena
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Clinical Improvement ◽  
Zinc Supplementation ◽  
Intervention Group ◽  
Persistent Asthma ◽  
Control Group ◽  
Fibroblast Growth ◽  
Asthma Control Test ◽  
Significant Difference

Background: Background The presence of remodeling process on the pathogenesis of asthma that involves some growth factors such as epidermal growth factor (EGF) and fibroblast growth factor (FGF) causes the chronicity of the disease. The role of zinc on the pathogenesis of asthma is being widely investigated. This study aimed to analyze the correlation between EGF and FGF2 and clinical improvement of asthma after  zinc supplementation.Methods: A quasi-experimental study was conducted in Outpatient Clinic Dr. Soetomo Hospital. The samples were persistent asthma patients from 6-15 years old who received controller therapy. The samples were divided into 2 groups, those who received zinc supplementation as the intervention group, and who received pacebo as the control. EGF and FGF2 plasma level of both groups were measured, and clinical improvement was evaluated with Childhood Asthma Control Test (C-ACT).Results: There were 11 patients who received zinc supplementation and 12 patients in the control group. There was a significant difference (p = 0.000) on the increase of EGF level in the intervention group (55.59 ± 6.48) than the control (5.35 ± 5.55). There was a significant difference (p = 0.000) on the increase of the FGF2 level in the intervention group (6.37 ± 1.41) than the control (0.72 ± 0.48). The increase of EGF (r = 0.592; p = 0.003) and FGF2 (r = 0.607; p = 0.002) would be followed by the increase of C-ACT scores.Conclusion: Zinc supplementation increase EGF and FGF2 levels. This improvement is correlated with clinical improvement of patients.

Low Serum Levels of Fibroblast Growth Factor 2 in Gunn Rats: A Hyperbilirubinemia Animal Model of Schizophrenic Symptoms

2020 ◽  
Vol 19 (7) ◽  
pp. 503-508
Author(s):  
Maiko Hayashida ◽  
Sadayuki Hashioka ◽  
Kenji Hayashida ◽  
Shoko Miura ◽  
Keiko Tsuchie ◽  
...  
Keyword(s):  
Animal Model ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Wistar Rats ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Normal Strain ◽  
Fibroblast Growth ◽  
Gunn Rats

Background: Fibroblast growth factor (FGF) 2 (also referred to as basic FGF) is a multifunctional growth factor that plays a pivotal role in the pro-survival, pro-migration and pro-differentiation of neurons. Method: Because alterations in FGF2 levels are suggested to contribute to the pathogenesis schizophrenia, we investigated serum levels of FGF2 in the Gunn rat, a hyperbilirubinemia animal model of schizophrenic symptoms. Results: The enzyme-linked immunosorbent assay showed that the serum levels of FGF2 in Gunn rats were 5.09 ± 0.236 pg/mL, while those in the normal strain Wistar rats were 11.90 ± 2.142 pg/mL. The serum FGF2 levels in Gunn rats were significantly lower than those in Wistar rats. We also measured serum levels of unconjugated bilirubin (UCB) and found a significant negative correlation between UCB and FGF2 at serum levels in all the rats studied. Conclusion: Since it is known that FGF2 regulates dopaminergic neurons and have anti-neuroinflammatory effects, our finding suggests that low FGF2 levels may contribute to the pathogenesis of schizophrenia, in which disbalanced dopamin-ergic signaling and neuroinflammation are supposed to play certain roles.

scholarly journals Effect of Fibroblast Growth Factor 21 on the Expression of TLR4 and BAMBI Genes in Cholesterol-Treated Human Hepatic Stellate Cells

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Elham Shakerian ◽  
Narges Mohammad Taghvaei ◽  
Zohre Askari ◽  
Reza Afarin
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Fibroblast Growth Factor ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Fibroblast Growth Factor 21 ◽  
Control Group ◽  
Type I ◽  
Fibroblast Growth ◽  
Human Hscs

Background: Activated hepatic stellate cells (HSCs) are the primary mediators in the progression of hepatic fibrosis. The activation of toll-like receptor 4 (TLR4) signaling leads to the downregulation of the transmembrane inhibitory transforming growth factor-beta (TGF-β) pseudoreceptor BMP and activin membrane-bound inhibitor (BAMBI) on HSCs. Fibroblast growth factor 21 (FGF21) is a natural secretory protein in the body with effects, such as the reduction of fat accumulation and oxidation of lipids; however; no study has investigated FGF21 ability to prevent the progression of liver fibrosis. Objectives: This study aimed to examine the beneficial effects of FGF21 to reduce cholesterol-activated human HSCs. Methods: The human HSCs were incubated in media containing different concentrations of cholesterol, including 25, 50, 75, 100, 125, and 150 μM, for 24 h and then incubated with FGF21 for 24 h. Total ribonucleic acids were extracted and reversely transcribed into complementary deoxyribonucleic acid. A quantitative real-time polymerase chain reaction was performed in this study. Results: The results showed that the messenger ribonucleic acid (mRNA) expression of TGF-β, collagen, type I, alpha 1 (collagen1α), and TLR4 genes increased significantly in the presence of cholesterol (75 and 100 μM), compared to that of the control group (* P < 0.05, ** P < 0.01, and *** P < 0.001); nevertheless, the mRNA expression of the BAMBI gene significantly reduced, compared to that of the control group (* P < 0.05). The FGF21 significantly reduced the mRNA expression of TGF-β, collagen1α, and TLR4 genes (# P < 0.05). The mRNA expression of the BAMBI gene significantly increased with FGF21 (# P < 0.05). Conclusions: It was concluded that the treatment with FGF21 reduces the cholesterol-activated HSCs by decreasing the mRNA expression of the TLR4, TGF-β, and collagen1α genes and increasing the mRNA expression of the BAMBI gene.

Regenerative efficacy of fibroblast growth factor for the treatment of aged vocal fold: From animal model to clinical application

2020 ◽  
Vol 46 (1) ◽  
pp. 131-137 ◽  
Author(s):  
Myung Jin Ban ◽  
Seung Chul Lee ◽  
Jae Hong Park ◽  
Ki Nam Park ◽  
Hee Kyung Kim ◽  
...  
Keyword(s):  
Animal Model ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Clinical Application ◽  
Vocal Fold ◽  
Fibroblast Growth

scholarly journals Elevated Fibroblast Growth Factor 23 Concentration: Prediction of Mortality among Chronic Kidney Disease Patients

2015 ◽  
Vol 6 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Shahanas Chathoth ◽  
Samir Al-Mueilo ◽  
Cyril Cyrus ◽  
Chittibabu Vatte ◽  
Awatif Al-Nafaie ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Control Group ◽  
Phosphorus Metabolism ◽  
Fibroblast Growth ◽  
Saudi Population ◽  
Fgf23 Level

Background: The osteocyte-derived hormone, fibroblast growth factor 23 (FGF23), regulates the phosphorus metabolism and suppresses 1,25-dihydroxyvitamin D production, thereby mitigating hyperphosphatemia in patients with renal disorders. An elevated FGF23 level is suggested to be an early biomarker of altered phosphorus metabolism in the initial stages of chronic kidney disease (CKD) and acts as a strong predictor of mortality in dialysis patients. In the Saudi population, there is no report on the FGF23 level in CKD patients to date. This study aims to estimate the plasma FGF23 levels in the Saudi population and to correlate it with its clinical manifestations in order to ascertain its role in the pathogenesis of CKD patients. Methods: The FGF23 level in the plasma samples was determined using ELISA in a diverse cohort of 89 cases with stage 3-5 CKD and 100 healthy subjects. The plasma FGF23 level was correlated with other biochemical parameters. Results: The results revealed that the FGF23 level was markedly elevated among CKD patients compared to the control group, and a significant inverse correlation was observed between the FGF23 level and glomerular filtration rate. FGF23 elevation was approximately 40-fold among stage 5 patients compared to the control, while the elevation of phosphate, parathyroid hormone (PTH) and alkaline phosphatase was 2-, 3- and 8-fold in this stage, respectively. Conclusion: Elevated FGF23 levels may have a strong correlation with the disease pathogenesis. In addition, FGF23 might be a future therapeutic target to intervene against the progression of CKD as well as to increase patient survivability.

scholarly journals MicroRNA-145 repairs infarcted myocardium by accelerating cardiomyocyte autophagy

2015 ◽  
Vol 309 (11) ◽  
pp. H1813-H1826 ◽  
Author(s):  
Kenshi Higashi ◽  
Yoshihisa Yamada ◽  
Shingo Minatoguchi ◽  
Shinya Baba ◽  
Masamitsu Iwasa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor Receptor ◽  
Rabbit Model ◽  
Growth Factor Receptor ◽  
Control Group ◽  
Fibroblast Growth ◽  
H9c2 Cells ◽  
Phosphorylated Akt ◽  
Cardiomyocyte Autophagy

We investigated whether microRNA-145 (miR-145) has a cardioprotective effect in a rabbit model of myocardial infarction (MI) and in H9c2 rat cardiomyoblasts. Rabbits underwent 30 min of coronary occlusion, followed by 2 days or 2 wk of reperfusion. Control microRNA (control group; 2.5 nmol/kg, n = 10) or miR-145 (miR-145 group, 2.5 nmol/kg, n = 10) encapsulated in liposomes was intravenously administered immediately after the start of reperfusion. H9c2 rat cardiomyoblasts were transfected with miR-145. The MI size was significantly smaller in the miR-145 group than in the control group at 2 days and 2 wk post-MI. miR-145 had improved the cardiac function and remodeling at 2 wk post-MI. These effects were reversed by chloroquine. Western blot analysis showed that miR-145 accelerated the transition of LC3B I to II and downregulated p62/SQSTM1 at 2 days or 2 wk after MI, but not at 4 wk, and activated Akt in the ischemic area at 2 days after MI. miR-145 inhibited the growth of H9c2 cells, accelerated the transition of LC3B I to II, and increased phosphorylated Akt in the H9c2 cells at 2 days after miR-145 transfection. Antagomir-145 significantly abolished the morphological change, the transition of LC3B I to II, and the increased phosphorylated Akt induced by miR-145 in H9c2 cells. We determined fibroblast growth factor receptor substrate 2 mRNA to be a target of miR-145, both in an in vivo model and in H9c2 cells. In conclusion, post-MI treatment with miR-145 protected the heart through the induction of cardiomyocyte autophagy by targeting fibroblast growth factor receptor substrate 2.

scholarly journals Fibroblast Growth Factor-9 Activates c-Kit Progenitor Cells and Enhances Angiogenesis in the Infarcted Diabetic Heart

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Dinender Singla ◽  
Jing Wang
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Progenitor Cells ◽  
Cell Activation ◽  
Left Ventricular ◽  
Diabetic Heart ◽  
Fibroblast Growth ◽  
Sham Surgery ◽  
Left Ventricular Output ◽  
Fractional Shortening

We hypothesized that fibroblast growth factor-9 (FGF-9) would enhance angiogenesis via activating c-kit positive stem cells in the infarcted nondiabetic and diabetic heart. In brief, animals were divided into three groups: Sham, MI, and MI+FGF-9. Two weeks following MI or sham surgery, our data suggest that treatment with FGF-9 significantly diminished vascular apoptosis compared to the MI group in both C57BL/6 and db/db mice (p<0.05). Additionally, the number of c-kit+ve/SMα-actin+vecells and c-kit+ve/CD31+vecells were greatly enhanced in the MI+FGF-9 groups relative to the MI suggesting FGF-9 enhances c-Kit cell activation and their differentiation into vascular smooth muscle cells and endothelial cells, respectively (p<0.05). Histology shows that the total number of vessels were quantified for all groups and our data suggest that the FGF-9 treated groups had significantly more vessels than their MI counterparts (p<0.05). Finally, echocardiographic data suggests a significant improvement in left ventricular output, as indicated by fractional shortening and ejection fraction in both nondiabetic and diabetic animals treated with FGF-9 (p<0.05). Overall, our data suggests FGF-9 has the potential to attenuate vascular cell apoptosis, activate c-Kit progenitor cells, and enhance angiogenesis and neovascularization in C57BL/6 and db/db mice leading to improved cardiac function.

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