scholarly journals Salivary growth factors in patients with chronic periodontitis

2021 ◽  
Vol 102 (5) ◽  
pp. 636-641
Author(s):  
V V Bazarnyi ◽  
L G Polushina ◽  
E A Sementsova ◽  
A Yu Maksimova ◽  
E N Svetlakova ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factors ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Chronic Periodontitis ◽  
Vascular Endothelial ◽  
Nerve Growth ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

Aim. To determine the clinical value of the growth factors concentration in the oral fluid in patients with mild chronic periodontitis. Methods. A prospective study including 30 patients with chronic periodontitis and 20 healthy volunteers was conducted. The diagnosis was made based on standard clinical and radiological criteria. Nerve growth factor (NGF-), hepatocyte growth factor (HGF), epidermal growth factor (EGF), vascular endothelial growth factor A (VEGF-A), platelet-derived growth factor BB (PDGF-BB) were determined in oral fluid samples by using multiparametric fluorescence analysis with magnetic microspheres (xMAP technology, Luminex 200, USA). Statistical analysis was performed using nonparametric measures: median (Me) and interquartile range (Q1, Q3). Receiver operating characteristic (ROC) analysis was used to determine the clinical value of the parameters. Results. The chronic periodontitis was accompanied by an increase in the level of nerve growth factor- by 2.2 times, epidermal growth factor by 3 times, vascular endothelial growth factor A by 1.9 times (p 0.05) compared with the control. The platelet-derived growth factor BB concentration did not change. Using the ROC analysis, diagnostic sensitivity and diagnostic specificity of the studied parameters were determined: 89.1 and 91.1% for nerve growth factor , 92.3 and 96.1% for epidermal growth factor, 87.1 and 95.3% for vascular endothelial growth factor A, respectively. Conclusion. Salivary growth factors (nerve growth factor , epidermal growth factor, vascular endothelial growth factor A) can be considered as potential biomarkers of mild chronic periodontitis.

Egr-1 gene is induced by the systemic administration of the vascular endothelial growth factor and the epidermal growth factor

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1772-1781
Author(s):  
Lixin Liu ◽  
Jo C. Tsai ◽  
William C. Aird
Keyword(s):  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

Egr-1 is a transcription factor that couples short-term changes in the extracellular milieu to long-term changes in gene expression. In cultured endothelial cells, the Egr-1 gene has been shown to respond to a variety of extracellular signals. However, the physiological relevance of these findings remains unclear. To address this question, the growth factor-mediated response of the Egr-1 gene under in vivo conditions was analyzed. To that end, either vascular endothelial growth factor (VEGF) or epidermal growth factor (EGF) was injected into the intraperitoneal cavity of mice. Growth factors were delivered to all tissues examined, as evidenced by the widespread distribution of I125-labeled growth factors and the phosphorylation of their respective receptors. In Western blot analyses of whole-tissue extracts, Egr-1 protein levels were shown to be induced in the heart, brain, liver, and spleen of VEGF-treated mice, and in the heart, lung, brain, liver and skeletal muscle of EGF-treated animals. Changes in Egr-1 levels did not correlate with changes in receptor phosphorylation or ERK1/2 phosphorylation. In Northern blot analyses, VEGF induced Egr-1 mRNA levels in all tissues examined except lung and kidney, whereas EGF led to increased transcripts in all tissues except kidney. In immunofluorescence studies, VEGF induced Egr-1 in microvascular endothelial cells of the heart and liver, and EGF induced Egr-1 in the microvascular bed of skeletal muscle. Taken together, these results suggest that the Egr-1 gene is differentially regulated in response to systemically administered VEGF and EGF.

Egr-1 gene is induced by the systemic administration of the vascular endothelial growth factor and the epidermal growth factor

Blood ◽  
2000 ◽  
Vol 96 (5) ◽  
pp. 1772-1781 ◽  
Author(s):  
Lixin Liu ◽  
Jo C. Tsai ◽  
William C. Aird
Keyword(s):  
Skeletal Muscle ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Mrna Levels ◽  
Vascular Endothelial ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

Abstract Egr-1 is a transcription factor that couples short-term changes in the extracellular milieu to long-term changes in gene expression. In cultured endothelial cells, the Egr-1 gene has been shown to respond to a variety of extracellular signals. However, the physiological relevance of these findings remains unclear. To address this question, the growth factor-mediated response of the Egr-1 gene under in vivo conditions was analyzed. To that end, either vascular endothelial growth factor (VEGF) or epidermal growth factor (EGF) was injected into the intraperitoneal cavity of mice. Growth factors were delivered to all tissues examined, as evidenced by the widespread distribution of I125-labeled growth factors and the phosphorylation of their respective receptors. In Western blot analyses of whole-tissue extracts, Egr-1 protein levels were shown to be induced in the heart, brain, liver, and spleen of VEGF-treated mice, and in the heart, lung, brain, liver and skeletal muscle of EGF-treated animals. Changes in Egr-1 levels did not correlate with changes in receptor phosphorylation or ERK1/2 phosphorylation. In Northern blot analyses, VEGF induced Egr-1 mRNA levels in all tissues examined except lung and kidney, whereas EGF led to increased transcripts in all tissues except kidney. In immunofluorescence studies, VEGF induced Egr-1 in microvascular endothelial cells of the heart and liver, and EGF induced Egr-1 in the microvascular bed of skeletal muscle. Taken together, these results suggest that the Egr-1 gene is differentially regulated in response to systemically administered VEGF and EGF.

Fortgeschrittenes medulläres Schilddrüsenkarzinom: Vandetanib verbessert das progressionsfreie Überleben

2012 ◽  
Vol 03 (02) ◽  
pp. 93-92
Author(s):  
Alexander Kretzschmar
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Phase Iii ◽  
Vascular Endothelial ◽  
Medulläres Schilddrüsenkarzinom ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

Vandetanib ist ein oraler Hemmer des RET-Kinase-, VEGF (Vascular Endothelial Growth Factor Receptor)- und EGFR (Epidermal Growth Factor Receptor)-Signalwegs. In einer zulassungsrelevanten, randomisierten, doppelblinden, placebokontrollierten Phase- III-Studie verlängerte der Tyrosinkinasehemmer das progressionsfreie Überleben (PFS) signifikant länger als Placebo.

scholarly journals Changes in Gene Expression in Rat Tissues during Toxoplasmosis

2021 ◽  
Vol 6 (2) ◽  
pp. 236-241
Author(s):  
E. S. Pashinskaya ◽  
Keyword(s):  
Gene Expression ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Lung Tissue ◽  
Rat Tissues ◽  
Vascular Endothelial ◽  
Epidermal Growth ◽  
Endothelial Growth Factor ◽  
Brain Tissues

The purpose of the study is to study changes in gene expression in rat tissues during toxoplasmosis. Materials and methods. The experiment was conducted on 70 Wistar females weighing 170-220 grams. To achieve this goal, the expression of the proto-oncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI, vascular endothelial growth factor (VEGF) and anti-oncogene TP53 was determined in comparison with the reference genes β-actin (ACTB) and GAPDH by PCR analysis in the tissues of 10 healthy female rats and 60 infected with toxoplasma. RNA isolation was performed by the column method using the ReliaPrep RNA Cell Miniprep System (Promega Corporation, USA). The quality of the isolated RNA was evaluated spectrophotometrically. Reverse transcription was performed using M-MuLV RT (New England BioLabs Inc, USA). Primers specific to the genes were prepared using Primer3 and the NCBI Nucleotide database. Amplification was performed on a Real-Time PCR Detection System CFX96 thermal cycler (Bio-Rad, USA), using a qPCRmix-HS SYBR PCR mixture (Eurogen, Russia). Comparative expression of the studied genes was carried out after normalization of each of the samples to the level of the control genes GAPDH and ACTIN-β. Expression analysis was performed by qbase+ and CFX Maestro. Statistical processing of the obtained data was carried out using the program Statistica 10.0. Results and discussion. Toxoplasma increases the expression of survivin (BIRC5) in lung tissue to 0.013 relative units, in liver – to 0.038 relative units, in spleen – to 0.061 relative units, and in brain – to 0.050 relative units. VEGF expression in lungs increased to 0.034 relative units, in liver – to 0.041 relative units, in spleen – to 0.063 relative units, in brain tissues – to 0.080 relative units. There was an increase in the expression of ErbB-2/HER2-Neu in lung tissue to 0.436 relative units, in liver – to 0.259 relative units, in spleen – to 0.271 relative units, and in brain – to 0.131 relative units. GLI expression in lung tissues after toxoplasma infection increased to 0.113 relative units, in liver – to 0.188 relative units, in spleen – to 0.388 relative units, and in brain tissues – to 0.459 relative units. An increase in the expression of the anti-oncogene TP53 in the tissues of the lungs to 0.171 relative units, liver – to 0.295, spleen – to 0.408, and brain – to 0.259 relative units was revealed. Conclusion. It has been shown that toxoplasma can cause an increase in the expression of the proto-oncogenes survivin (BIRC5), epidermal growth factor (ErbB-2/HER2-Neu), GLI and vascular endothelial growth factor (VEGF) with simultaneous enhancement of the anti-oncogene TP53

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