Tea catechins inhibit angiogenesis in vitro, measured by human endothelial cell growth, migration and tube formation, through inhibition of VEGF receptor binding

2002 ◽  
Vol 180 (2) ◽  
pp. 139-144 ◽  
Author(s):  
Takako Kondo ◽  
Toshiro Ohta ◽  
Koichi Igura ◽  
Yukihiko Hara ◽  
Kazuhiko Kaji
Keyword(s):  
Endothelial Cell ◽  
Cell Growth ◽  
Receptor Binding ◽  
Tube Formation ◽  
Human Endothelial Cell ◽  
Vegf Receptor ◽  
Tea Catechins ◽  
Endothelial Cell Growth

Organization and chromosomal localization of the human platelet-derived endothelial cell growth factor gene

1991 ◽  
Vol 11 (4) ◽  
pp. 2125-2132
Author(s):  
K Hagiwara ◽  
G Stenman ◽  
H Honda ◽  
P Sahlin ◽  
A Andersson ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Human Platelet ◽  
Angiogenic Factor ◽  
Transcription Start Sites ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth

Human platelet-derived endothelial cell growth factor (hPD-ECGF) is a novel angiogenic factor which stimulates endothelial cell growth in vitro and promotes angiogenesis in vivo. We report here the cloning and sequencing of the gene for hPD-ECGF and its flanking regions. This gene is composed of 10 exons dispersed over a 4.3-kb region. Its promoter lacks a TATA box and a CCAAT box, structures characteristic of eukaryotic promoters. Instead, six copies of potential Sp1-binding sites (GGGCGG or CCGCCC) were clustered just upstream of the transcription start sites. Southern blot analysis using genomic DNAs from several vertebrates suggested that the gene for PD-ECGF is conserved phylogenetically among vertebrates. The gene for hPD-ECGF was localized to chromosome 22 by analysis of a panel of human-rodent somatic cell hybrid lines.

scholarly journals Intrauterine growth restriction decreases pulmonary alveolar and vessel growth and causes pulmonary artery endothelial cell dysfunction in vitro in fetal sheep

2011 ◽  
Vol 301 (6) ◽  
pp. L860-L871 ◽  
Author(s):  
Paul J. Rozance ◽  
Gregory J. Seedorf ◽  
Alicia Brown ◽  
Gates Roe ◽  
Meghan C. O'Meara ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Growth ◽  
Pulmonary Artery ◽  
Intrauterine Growth Restriction ◽  
Tube Formation ◽  
No Production ◽  
Vascular Growth ◽  
Intrauterine Growth ◽  
Pulmonary Artery Endothelial Cell

Intrauterine growth restriction (IUGR) increases the risk for bronchopulmonary dysplasia (BPD). Abnormal lung structure has been noted in animal models of IUGR, but whether IUGR adversely impacts fetal pulmonary vascular development and pulmonary artery endothelial cell (PAEC) function is unknown. We hypothesized that IUGR would decrease fetal pulmonary alveolarization, vascular growth, and in vitro PAEC function. Studies were performed in an established model of severe placental insufficiency and IUGR induced by exposing pregnant sheep to elevated temperatures. Alveolarization, quantified by radial alveolar counts, was decreased 20% ( P < 0.005) in IUGR fetuses. Pulmonary vessel density was decreased 44% ( P < 0.01) in IUGR fetuses. In vitro, insulin increased control PAEC migration, tube formation, and nitric oxide (NO) production. This response was absent in IUGR PAECs. VEGFA stimulated tube formation, and NO production also was absent. In control PAECs, insulin increased cell growth by 68% ( P < 0.0001). Cell growth was reduced in IUGR PAECs by 29% at baseline ( P < 0.01), and the response to insulin was attenuated ( P < 0.005). Despite increased basal and insulin-stimulated Akt phosphorylation in IUGR PAECs, endothelial NO synthase (eNOS) protein expression as well as basal and insulin-stimulated eNOS phosphorylation were decreased in IUGR PAECs. Both VEGFA and VEGFR2 also were decreased in IUGR PAECs. We conclude that fetuses with IUGR are characterized by decreased alveolar and vascular growth and PAEC dysfunction in vitro. This may contribute to the increased risk for adverse respiratory outcomes and BPD in infants with IUGR.

Activation of a procollagenase by low-molecular-weight angiogenesis factor

1983 ◽  
Vol 3 (2) ◽  
pp. 171-177 ◽  
Author(s):  
Jacqueline B. Weiss ◽  
C. R. Hill ◽  
R. J. Davis ◽  
B. McLaughlin ◽  
K. A. Sedowofia ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Growth ◽  
Low Molecular Weight ◽  
Type I ◽  
Angiogenesis Factor ◽  
The Matrix ◽  
Endothelial Cell Growth

Avascular tumours have the ability to establish a blood supply for themselves by secreting a humoral factor which stimulates their host's endothelial cells to proliferate and to migrate towards the tumour source. The mechanism of action of such a humoral anglo-genesis factor is more than that of an endothelial-cell growth factor since it requires an oriented migration of cells towards the tumour. We report here the activation of pure skin-fibroblast procollagenase by a low-molecular-weight angiogenesis factor capable of stimulating endothelial-cell growth in vitro. The activation was observed when either Type I or III collagen was used as substrate. It is suggested that at least one function of angiogenesis factor is to promote limited degradation of the connective tissue through which it passes causing channeling in the matrix along which stimulated endothelial cells may

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