Real-time immuno-polymerase chain reaction in a 384-well format: Detection of vascular endothelial growth factor and epidermal growth factor-like domain 7

2014 ◽  
Vol 463 ◽  
pp. 61-66 ◽  
Author(s):  
Jianhuan Zhang ◽  
Jean-Michel Vernes ◽  
Jennifer Ni ◽  
Christopher Nelson ◽  
Anne Wong ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Polymerase Chain Reaction ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Real Time ◽  
Vascular Endothelial ◽  
Chain Reaction ◽  
Epidermal Growth ◽  
Polymerase Chain ◽  
Endothelial Growth Factor

Effects of shRNA Targeting Maspin on the Invasion of Extravillous Trophoblast Cell

2017 ◽  
Vol 34 (10) ◽  
pp. 0966-0973 ◽  
Author(s):  
Xinwei Shi ◽  
Qing Liu ◽  
Hao Liu ◽  
Dongrui Deng ◽  
Fuyuan Qiao ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Polymerase Chain Reaction ◽  
Growth Factor ◽  
Trophoblast Cell ◽  
Extravillous Trophoblast ◽  
Vascular Endothelial ◽  
Chain Reaction ◽  
Maspin Expression ◽  
Polymerase Chain ◽  
Endothelial Growth Factor

Objective Hypomethylation of the maspin gene results in increased expression of maspin in preeclamptic placentas. However, maspin gene function and the molecular aspects in placentation remain largely unclear. The study was designed to investigate the effects of maspin on the invasion of extravillous trophoblast cell line (TEV-1) and the molecular mechanism. Study Design We cloned short hairpin RNA (shRNA) targeting maspin gene into plasmid pGenesil-1.1 eukaryotic expression vector and then transfected it using adenovirus. The methylation rates in the maspin gene were detected by bisulfite sequencing polymerase chain reaction; the invasive ability of trophoblast cells was examined by Transwell chamber assay; the mRNA and protein expression of maspin and some invasive related gene was detected by reverse transcription-polymerase chain reaction and Western blot analysis. Results After the maspin expression was successfully knocked down, the methylation rates in the maspin gene were significantly increased, and the number of cells invading through Matrigel (Corning Life Sciences and BD Biosciences) was obviously increased. The mRNA levels of vascular endothelial growth factor-A (VEGF-A), vascular endothelial growth factor-C (VEGF-C), and matrix metalloproteinase-2 (MMP2) were increased significantly. Conclusion Using shRNA technology, this study further verified that maspin gene methylation could decrease maspin expression and inhibit the invasion of TEV-1 cells through VEGF-A, VEGF-C, and MMP2.

scholarly journals Expression of mRNA vascular endothelial growth factor in hypospadias patients

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Prahara Yuri ◽  
Gunadi ◽  
Rahmadani P. Lestari ◽  
Firly P. Fardilla ◽  
Ishandono Dachlan
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Polymerase Chain Reaction ◽  
Growth Factor ◽  
Fold Change ◽  
Vascular Endothelial ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Distal Hypospadias ◽  
Endothelial Growth Factor ◽  
Larger Sample

Abstract Background Hypospadias is a relatively common genital anomaly in humans, usually followed by inelastic dartos that causes penile chordee. Vascular endothelial growth factor (VEGF) is strongly linked to the viscoelasticity of tissues and their elastic phase. This study aimed to evaluate VEGF expressions in (1) fascia dartos between hypospadias and controls and (2) chordee severity. Methods This prospective cohort study involved 65 specimens from patients with hypospadias and ten specimens from controls. The samples were analyzed by quantitative real-time polymerase chain reaction (qPCR) for VEGF expression. Results The expressions of VEGF were not different between proximal and distal hypospadias patients and controls (fold change: distal − 0.25; fold change: proximal − 0.2; p = 0.664). The scaled expressions related to chordee severity were mild − 0.1; moderate 0.1; severe − 0.25 (p = 0.660). Conclusions VEGF expressions might not affect the severity of hypospadias and chordee, implying the pathogenesis is complex involving many growth factors. Further study with a larger sample size is necessary to clarify and confirm our findings.

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

Expression of vascular endothelial growth factor A isoforms is dysregulated in women with endometriosis

2018 ◽  
Vol 30 (4) ◽  
pp. 651 ◽  
Author(s):  
Kevin Danastas ◽  
Emily J. Miller ◽  
Alison J. Hey-Cunningham ◽  
Christopher R. Murphy ◽  
Laura A. Lindsay
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Quantitative Polymerase Chain Reaction ◽  
Polymerase Chain Reaction Analysis ◽  
Vascular Endothelial ◽  
Chain Reaction ◽  
Natural Production ◽  
Polymerase Chain ◽  
Endothelial Growth Factor ◽  
Natural Expression

Angiogenesis is a critical step in the development of ectopic lesions during endometriosis. Although total vascular endothelial growth factor (VEGF) A is elevated in the peritoneal fluid of women with endometriosis, there are contradictory reports on how levels of total endometrial VEGFA are altered in this disease. Furthermore, limited research is available on different VEGFA isoforms in women with endometriosis. Thus, the aim of the present study was to analyse levels of various VEGFA isoforms in women with and without endometriosis at different stages of the menstrual cycle. Quantitative polymerase chain reaction analysis showed that total VEGFA was highest during menstruation in endometriosis compared with controls (P = 0.0373). VEGF121 and VEGF189 were similarly highest during menstruation in endometriosis compared with controls (P = 0.0165 and 0.0154 respectively). The present study is also the first to identify the natural expression of VEGF111 in human tissue, which is also highest during menstruation in endometriosis (P = 0.0464). This discovery of the natural production of VEGF111 in human endometrium, as well as the upregulation of VEGFA isoforms during menstruation in endometriosis, may shed further light on the development and progression of the disease, and improve our understanding of the regulation of endometrial angiogenesis.

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