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.

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 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.

scholarly journals Decoding the Genetic Alterations in Genes of Fibroblast Growth Factor Family and Their Possible Association with HNSCC

2021 ◽  
pp. 698-710
Author(s):  
A. Akshaya ◽  
J. Vijayashree Priyadharsini ◽  
A. S. Smiline Girija ◽  
P. Sankar Ganesh ◽  
Nidhi Poddar
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Demographic Data ◽  
Primary Tumour ◽  
Genetic Alterations ◽  
Fibroblast Growth ◽  
Heparin Binding ◽  
Fibroblast Growth Factor Family ◽  
Significant Difference ◽  
Cancer Phenotypes

Introduction: HNSCC is a type of cancer in the oral and pharynx region. Several mutations/variations are observed in these cancer phenotypes. Fibroblast growth factor belongs to the family of heparin binding growth factors. FGFs are multifunctional proteins with a wide variety of effects; they are most commonly mitogens. Their expression pattern correlates with invasion of HNSCC. Aim: To assess the genetic alterations in genes of the fibroblast growth factor family and their association with HNSCC. Materials and Methods: The demographic data and samples of 528 HNSCC patients was collected from the cBioportal database. Oncoprint analysis was done to assess the amplification and genetic alterations of the members of the FGF gene family. String analysis was performed to evaluate the protein-protein interaction. The information about previous reported mutation and correlation with novel and reported mutation was obtained using GnomAD analysis. Results and Discussion: FGF3,4 and 19 genes showed maximum variation (25%). FGF4 and FGF19 genes showed maximum amplification in addition to deletion mutation. Excitingly FGF3, FGF4 and FGF19 genes showed similar amplification patterns in most of the HNSCC patients. Statistical significant difference in the gene expression of FGF3 9.578 x 10-3 observed between normal and primary tumour. S.  Findings showed many novel mutations and also 4 reported mutations ie:FGF1, FGF12, FGF20, FGF21 Conclusion: Our present study concludes that more evidence is required to confirm their association with HNSCC.

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.

Fibroblast Growth Factor 21 in Patients with Acromegaly

2017 ◽  
Vol 125 (10) ◽  
pp. 649-654 ◽  
Author(s):  
Jowita Halupczok-Żyła ◽  
Aleksandra Jawiarczyk-Przybyłowska ◽  
Marek Skrzypski ◽  
Mathias Strowski ◽  
Marek Bolanowski
Keyword(s):  
Growth Factor ◽  
Disease Activity ◽  
Fibroblast Growth Factor ◽  
Body Mass ◽  
Hdl Cholesterol ◽  
Fibroblast Growth Factor 21 ◽  
Control Group ◽  
Fibroblast Growth ◽  
Anthropometric Parameters ◽  
Cholesterol Levels

Abstract Introduction The goal of the study was to investigate fibroblast growth factor-21 (FGF-21) levels in acromegalic patients in relation to the disease activity and to compare them with controls. Further, we aimed to evaluate the associations between FGF-21 and random growth hormone (GH), insulin-like growth factor-1 (IGF-1), metabolic and anthropometric parameters. Materials and methods The study group consisted of 50 acromegalic patients divided into 3 subgroups on the basis of disease activity (AA – active acromegaly, CD – controlled disease, CA – cured acromegaly). 27 subjects were assigned to the control group (CG). Blood samples were obtained from all participants to assess FGF-21, GH, IGF-1, lipids, glucose and insulin levels. Body mass, body mass index and body composition were also evaluated. Results There were no statistically significant differences in FGF-21 concentrations across all groups despite of subjects classification. FGF-21 correlated positively with random GH in the groups: CA, CD+CA, AA+CD+CA (r=0.48, p=0.049; r=0.39, p=0.023; r=0.33, p=0.02; respectively); with IGF-1 in the AA+CD+CA group (r=0.29, p=0.041); with triglycerides in the following groups: CD, CD+CA, AA+CD+CA (r=0.63, p=0.08; r=0.44, p=0.01; r=0.37, p=0.007; respectively) and with age in the CG and CD+CA groups (r=0.41, p=0.029; r=0.42, p=0.029; respectively). There were statistically significant negative correlations between FGF-21 and HDL-cholesterol levels in the groups: CD, CD+CA, AA+CD+CA (r=-0.53, p=0.03; r=-0.37, p=0.032; r=-0.29, p=0.036, respectively). Conclusions FGF-21 levels were similar in patients with acromegaly compared to controls. However, our results indicate that FGF-21 may have a potential role in the development of acromegaly complications.

scholarly journals Plasma Concentrations of Vascular Endothelial Growth Factor and Basic Fibroblast Growth Factor in Lymphoproliferative Disorders

2005 ◽  
Vol 48 (1) ◽  
pp. 57-58 ◽  
Author(s):  
Lukáš Smolej ◽  
Ctirad Andrýs ◽  
Vladimír Maisnar ◽  
Luděk Pour ◽  
Jaroslav Malý
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Plasma Concentrations ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Vascular Endothelial ◽  
Fibroblast Growth ◽  
Endothelial Growth Factor

Angiogenesis plays a major role in the development and progression of haematological malignancies. In our study we measured plasma concentrations of key angiogenic activators vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) using comercially available sandwich enzyme-linked immunosorbent assay (ELISA) in 37 patients with lymphoid malignancies and 20 healthy donors. We found a statistically significant increase in bFGF concentrations in patients with B-cell chronic lymphocytic leukemia (B-CLL, n=18) compared to the control group (median 118.8 vs. 9.3 pg/ml, p<0.001). However, we didn’t find any significant difference in VEGF concentrations between B-CLL patients and the control group. There was also no significant increase in bFGF or VEGF in patients with multiple myeloma (n=7) and non-Hodgkin’s lymphoma (n=12). Our pilot study shows that measurement of angiogenic activators in plasma is a feasible and reproducible method of angiogenesis assessment. Larger studies are needed for correlation between serum and plasma concentrations and detailed statistical evaluation including the impact on patients’ survival.

scholarly journals SAT-046 Insulin-Like Growth Factor and Fibroblast Growth Factor 21 in Men with Klinefelter Syndrome

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Simon Chang ◽  
Rikke Hjortebjerg ◽  
Anders Bojesen ◽  
Mette Bjerre ◽  
Claus Hojbjerg Gravholt
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Klinefelter Syndrome ◽  
Protein A ◽  
Serum Levels ◽  
Fibroblast Growth Factor 21 ◽  
Control Group ◽  
Insulin Like Growth Factor ◽  
Fibroblast Growth ◽  
Igf System

Abstract Background: Men with 47, XXY Klinefelter syndrome (KS) commonly present with obesity, metabolic disorders, and insulin insensitivity. The insulin-like growth factor (IGF) system has pleiotropic effects including regulation of glucose metabolism. Fibroblast growth factor 21 (FGF21) is associated with weight loss and favourable metabolic changes, but patients with obesity or type 2 diabetes might be resistant to this effect despite presenting with increased levels. Aim: To describe levels of components in the IGF system and FGF21 among men with KS, either treated or not treated with testosterone supplementation therapy (TT), in comparison with control males. Methods: A total of 66 men with KS were included, 33 without current TT and 33 with current TT. A control group of 70 healthy age-matched males were included. Serum levels of insulin-like growth factor 1 (IGF-1), insulin-like growth factor-binding protein 3 (IGFBP3), pregnancy-associated plasma protein A (PAPP-A), FGF21, and fibroblast activation protein (FAP) were compared between the three groups applying the Kruskal-Wallis test. Results: Levels of (IGF-1 µg/L) were not different between the groups (median (25-75 %), untreated KS 162 (140-201.5), treated KS 165 (128.5-215), controls 176.5 (150.8-214.5), p=0.5). Similarly, FGF21 levels (ng/L) were comparable between the groups (median (25-75 %), untreated KS 84.7 (53.3-217.6), treated KS 97.2 (56.4-224.8), controls 100.3 (66.0-191.0), p=0.9). Levels of IGFBP3, PAPP-A and FAP were also found to be comparable between the groups (p≥0.2). Conclusion: This was the first study investigating FGF21 in men with KS. Our results indicate that regulation of the IGF-1 system and levels of FGF21 are not altered in men with KS compared with age-matched controls, and that TT in men with KS does not affect these systems.

scholarly journals Association study of five mutation in FGFR1 and FGFR2 genes in Indian children with craniosynostosis

Genetika ◽  
2013 ◽  
Vol 45 (3) ◽  
pp. 881-893
Author(s):  
Rajeev Pandey ◽  
Abid Ali ◽  
Minu Bajpai ◽  
Sukanya Gayan ◽  
Amit Singh
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Indian Population ◽  
Fibroblast Growth Factor Receptor ◽  
Growth Factor Receptor ◽  
Control Group ◽  
Paediatric Surgery ◽  
Fibroblast Growth ◽  
Indian Children ◽  
Western Population

Background: Craniosynostosis is one the major genetic disorder in children and it occurs in 1 per 2,200 live births. It may be define as abnormal premature fusion of the cranial sutures bones in children. Several causes have been reported that may have a possible role in the development of the disorder. Fibrinogen growth Factor 1(FGFR1) & fibroblast growth factor receptor 2 (FGFR2) show a vital role in developing the craniosynostosis in western population?s children but from India no report is available. The aim of this study was to investigate the association between mutation of FGFR1 and FGFR2 (IIIa and IIIb) genes with syndromic as well as non-syndromic craniosynostosis in Indian population. Methods: Retrospective analysis of our records from January 2008 to December 2012 was done. A total of Sixty three children (along with their parents) with craniosynostosis and Fifty one children with No-craniosynostosis (healthy school going children) attending the Monday out Patient Door (OPD) facility of the department of Paediatric Surgery, All India Institute of Medical Sciences (AIIMSs), Delhi, India were considered for the study. A restriction fragment length polymorphism (RFLP) polymerase chain reaction (PCR) was carried out for genotyping Fibrinogen growth Factor 1 (FGFR1) & fibroblast growth factor receptor 2 (FGFR2) mutations in all the participants. Results: There were 33 (80.4%) nonsyndromic cases of craniosynostosis while 8 (19.5%) were syndromic. Out of these 8 syndromic cases, 4 were Apert syndrome, 3 were Crouzon syndrome and 1 Pfeiffer syndrome. Phenotypically the most common nonsyndromic craniosynostosis was scaphocephaly (19, 57.7%) followed by plagiocephaly in (14, 42.3%). FGFR1 mutation (Pro252Arg) was seen in 1 (2.4%) case of nonsyndromic craniosynostosis while no association was noted either with FGFR1 or with FGFR2 (IIIa & IIIc) mutation in syndromic cases. None of the control group showed any mutation. Conclusion: Our study provides the strongest evidence that association of mutation of FGFR1, FGFR2 (IIIa & IIIb) with syndromic as well as nonsyndromic craniosynostosis does not exist in Indian population as seen in western population.

scholarly journals Thioredoxin-1 and Correlations of the Plasma Cytokines Regarding Aortic Valve Stenosis Severity

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1041
Author(s):  
Peteris Tretjakovs ◽  
Juris Lurins ◽  
Simons Svirskis ◽  
Gita Gersone ◽  
Dace Lurina ◽  
...  
Keyword(s):  
Growth Factor ◽  
Aortic Valve ◽  
Fibroblast Growth Factor ◽  
Aortic Valve Stenosis ◽  
Plasma Levels ◽  
Fibroblast Growth Factor 21 ◽  
Control Group ◽  
Fibroblast Growth ◽  
Local Inflammatory Response ◽  
Thioredoxin 1

Aortic valve stenosis (AS) develops not only with a pronounced local inflammatory response, but also oxidative stress is involved. The aim of this study was to evaluate the plasma levels of thioredoxin-1 (TRX1), myeloperoxidase (MPO), chemerin, growth differentiation factor 15 (GDF-15), angiopoietin-2 (Ang-2), vascular endothelial growth factor A (VEGF-A), fibroblast growth factor 2 (FGF-2), fibroblast growth factor 21 (FGF-21), and metalloproteinase (MMP)-1, -3, and -9 in acquired AS patients as well as to clarify the correlations of TXR1 and the plasma inflammatory biomarkers regarding AS severity. AS patients were classified into three groups: 16 patients with mild AS stenosis, 19 with moderate and 11 with severe AS, and 30 subjects without AS were selected as a control group. AS patients had significantly higher plasma levels of TRX1 compared to controls, but the highest difference was found in mild AS patients compared to the controls. We conclude that AS is associated with significantly increased plasma TRX1 levels, and TRX1 might serve as a specific and sensitive biomarker of AS. TRX1 and also chemerin, GDF-15, VEGF-A, FGF-2 and FGF-21 significantly correlate with AS severity degrees. TRX1 also showed positive association with FGF-2, VEGF-A, and MMP-3 in all AS patients.

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