scholarly journals Vascular Endothelial Growth Factor Induces Heparin-binding Epidermal Growth Factor-like Growth Factor in Vascular Endothelial Cells

1998 ◽  
Vol 273 (8) ◽  
pp. 4400-4405 ◽  
Author(s):  
Burak M. Arkonac ◽  
Lauren C. Foster ◽  
Nicholas E. S. Sibinga ◽  
Cam Patterson ◽  
Kaihua Lai ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Heparin Binding ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

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.

Effect of vascular endothelial growth factor and epidermal growth factor on iatrogenic apoptosis in human endothelial cells

2004 ◽  
Vol 67 (2) ◽  
pp. 277-284 ◽  
Author(s):  
Maria Cristina Vinci ◽  
Barbara Visentin ◽  
Federico Cusinato ◽  
Giovanni Battista Nardelli ◽  
Lucia Trevisi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Epidermal Growth ◽  
Endothelial Growth Factor

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.

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