scholarly journals A microarray analysis for genes regulated by interferon-τ in ovine luminal epithelial cells

Reproduction ◽  
2007 ◽  
Vol 134 (1) ◽  
pp. 123-135 ◽  
Author(s):  
Yizhen Chen ◽  
Eric Antoniou ◽  
Zhilin Liu ◽  
Leonard B Hearne ◽  
R Michael Roberts
Keyword(s):  
Epithelial Cells ◽  
Microarray Analysis ◽  
Vascular Endothelial ◽  
Cdna Microarray Analysis ◽  
Ruminant Species ◽  
Physiological Processes ◽  
Prostaglandin F ◽  
Immortalized Cell ◽  
Endothelial Growth Factor ◽  
Luminal Epithelial Cells

Interferon-τ (IFNT) is released by preimplantation conceptuses of ruminant species and prepares the mother for pregnancy. Although one important function is to protect the corpus luteum from the luteolytic activity of prostaglandin-F 2α, IFNT most likely regulates a range of other physiological processes in endometrium. Here, an immortalized cell line from ovine uterine luminal epithelial cells was treated with IFNT for either 8 or 24 h. RNA was subjected to cDNA microarray analysis, with RNA from untreated cells as the reference standard. Of 15 634 genes, 1274 (8%) were IFNT responsive atP<0.01 and 585 atP<0.001 to at least one treatment. Of the latter, 356 were up-regulated and 229 down-regulated. Increasing IFNT concentrations from 10 ng/ml to 10 μg/ml had minor effects, and most genes up- or down-regulated at 8 h were regulated similarly at 24 h. Although IFNT influences many genes implicated in antiviral activity and apoptosis, its action also likely regulates prostaglandin metabolism, growth factors and their receptors, apoptosis and the nuclear factor (NF)-κB cascade, extracellular matrix accretion, angiogenesis, blood coagulation, and inflammation. In particular, it increased mRNA concentrations of genes related to the vascular endothelial growth factor R2 pathway of angiogenesis and down-regulated ones associated with hypoxia. Two genes implicated in the antiluteolytic actions of IFNT (encoding cyclooxygenase-2 and the oxytocin receptor respectively) were down-regulated in response to all treatments. IFNT targets a complex range of physiological processes during the establishment of pregnancy.

scholarly journals cDNA microarray analysis of genes associated with ERBB2 (HER2/neu) overexpression in human mammary luminal epithelial cells

Oncogene ◽  
2003 ◽  
Vol 22 (17) ◽  
pp. 2680-2688 ◽  
Author(s):  
Alan Mackay ◽  
Chris Jones ◽  
Tim Dexter ◽  
Ricardo L A Silva ◽  
Karen Bulmer ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Microarray Analysis ◽  
Cdna Microarray ◽  
Cdna Microarray Analysis ◽  
Luminal Epithelial Cells

scholarly journals The type 2 vascular endothelial growth factor receptor recruits insulin receptor substrate-1 in its signalling pathway

2002 ◽  
Vol 368 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Duraisamy SENTHIL ◽  
Goutam GHOSH CHOUDHURY ◽  
Basant K. BHANDARI ◽  
Balakuntalam S. KASINATH
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Protein Synthesis ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Tyrosine Phosphorylation ◽  
Kinase Activity ◽  
Insulin Receptor Substrate ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Vascular endothelial growth factor (VEGF) isoforms exert their biological effects through receptors that possess intrinsic tyrosine kinase activity. Whether VEGF binding to its receptors recruits insulin receptor substrate (IRS) family of docking proteins to the receptor is not known. Following incubation of mouse kidney proximal tubular epithelial cells with VEGF, we observed an increase in tyrosine phosphorylation of several proteins, including one of 200kDa, suggesting possible regulation of phosphorylation of IRS proteins. VEGF augmented tyrosine phosphorylation of IRS-1 in kidney epithelial cells and rat heart endothelial cells in a time-dependent manner. In the epithelial cells, association of IRS-1 with type 2 VEGF receptor was promoted by VEGF. VEGF also increased association of IRS-1 with the p85 regulatory subunit of phosphoinositide 3-kinase (PI 3-kinase), and PI 3-kinase activity in IRS-1 immunoprecipitates was increased in VEGF-treated cells. Incubation of epithelial cells with antisense IRS-1 oligonucleotide, but not sense oligonucleotide, reduced expression of the protein and VEGF-induced PI 3-kinase activity in IRS-1 immunoprecipitates. Additionally, VEGF-induced protein synthesis was also impaired by antisense but not sense IRS-1 oligonucleotide. These data provide the first evidence that binding of VEGF to its type 2 receptor promotes association of IRS-1 with the receptor complex. This association may account for some of the increase in VEGF-induced PI 3-kinase activity, and the increase in de novo protein synthesis seen in renal epithelial cells.

Long-Term Follow-Up of Immunocytochemical Analysis of Vascular Endothelial Growth Factor (VEGF), and Its Two Receptors, VEGF-R1 (Flt-1) and VEGF-R2 (Flk-1/KDR), in Oesophagogastric Cancer

2013 ◽  
Vol 28 (1) ◽  
pp. 63-70 ◽  
Author(s):  
Ronan T. Gray ◽  
Mark E. O'Donnell ◽  
Perry Maxwell ◽  
James A. McGuigan ◽  
Gary M. Spence
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Lymphovascular Invasion ◽  
Prognostic Significance ◽  
Vascular Endothelial ◽  
Immunocytochemical Analysis ◽  
Endothelial Growth Factor ◽  
Oesophagogastric Cancer

Background The prognostic significance of immunocytochemical analysis of tumour vascular endothelial growth factor (VEGF) and its 2 receptors, VEGF-R1 and VEGF-R2, remains incompletely investigated in patients with oesophagogastric cancer. Methods Patients undergoing surgical resection were prospectively recruited between February 1999 and August 2000. Immunocytochemical analysis of VEGF, VEGF-R1 (Flt-1) and VEGF-R2 (Flk-1/KDR) was undertaken using validated techniques. Patients were followed up over a 10-year period using the Northern Ireland Cancer Registry. Results Sixty-one patients were recruited (male=45, 73.8%) with a median age of 66.0 years (range 39-83). Forty-seven (77.0%) adenocarcinomas and 14 (23.0%) squamous cell carcinomas were resected. UICC tumour staging was: stage I=14.7%, II=24.6%, III=54.1% and IV=6.6%. VEGF, VEGF-R1 and VEGF-R2 were over-expressed in tumour epithelial cells. VEGF-R2 expression was decreased in the presence of lymphovascular invasion and higher tumour grade. The 10-year survival rate was 19.7% (n=12) with a median follow-up of 808 (IQR 356-2313) days. On univariate analysis only lymphovascular invasion significantly predicted poor prognosis in this cohort (p=0.05). Conclusion VEGF, VEGF-R1 and VEGF-R2 were over-expressed in tumour epithelial cells. VEGF-R2 expression was decreased in the presence of more aggressive pathological variables. Larger studies are required to assess the prognostic significance of these biomarkers in oesophagogastric cancer.

scholarly journals In Vitro Study on the Regulation of Annexin IV and VEGF by hCG in the Human Endometrium

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Shaoyuan Xu ◽  
Jie Li ◽  
Xiaoyan Chen ◽  
Beiyu Liu
Keyword(s):  
Epithelial Cells ◽  
In Vitro Study ◽  
Control Group ◽  
Vascular Endothelial ◽  
Vegf Mrna ◽  
Endometrial Cells ◽  
Mrna And Protein Expression ◽  
Endothelial Growth Factor ◽  
Annexin Iv

Objective. Whether changes in vascular endothelial growth factor (VEGF) and annexin IV during implantation are regulated through the LH/hCG-R needs further research. To investigate the mechanism of hCG on the expression of annexin IV and VEGF in human endometrial cells. Methods. Endometrial cells were isolated and identified from human specimens. The proportion of glandular and epithelial cells was analyzed. Annexin IV and VEGF were analyzed by qRT-PCR (mRNA), western blot (proteins), and immunohistochemistry (proteins). Protein location was identified by immunohistochemistry. The cells were cultured with hCG, hCG/PD98059 (a MAPK inhibitor), or no treatment (control). Results. The proportions between the glandular epithelial cells and stromal cells at inoculation and when adding hCG were 25.8 ± 0.2% and 27.8 ± 0.04%, respectively ( P > 0.05 ). LH/hCG-R, annexin IV, and VEGF were found in the cytoplasm of endometrial cells. After 2, 6, 12, and 24 h of hCG treatment, compared with 1 h, VEGF mRNA was increased by 1.25-fold, 3.19-fold, 4.21-fold, and 4.86-fold and annexin IV by 2.23-fold, 3.37-fold, 5.14-fold, and 5.02-fold. Compared with the control group, annexin IV mRNA and protein were increased in the hCG and hCG/PD98059 groups (mRNA/protein: 1.99-fold/1.80-fold and 2.33-fold/1.93-fold, P < 0.05 ). Compared with the control group, VEGF mRNA and protein were increased in the hCG group (mRNA/protein: 2.30-fold/1.86-fold), but not in the hCG/PD98059 group. Conclusion. hCG could upregulate the mRNA and protein expression of annexin IV and VEGF. The upregulation of annexin IV by hCG could not be inhibited by PD98059, but the upregulation of VEGF by hCG could.

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