Stimulation of cultured endothelial cells by endothelial cell growth factor and heparin

1986 ◽  
Vol 14 (6) ◽  
pp. 1048-1049
Author(s):  
TIMOTHY C. RICHARDSON ◽  
STEVEN A. HUMM
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Cultured Endothelial Cells ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth ◽  
Stimulation Of

scholarly journals CCN2 activates ERK-signaling via integrin αv and enhances the interaction of ERK and DUSP6 in lymphatic endothelial cells

2021 ◽  
Author(s):  
Shiho Hashiguchi ◽  
Tomoko Tanaka ◽  
Ryosuke Mano ◽  
Seiji Kondo ◽  
Shohta Kodama
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Vascular Endothelial Cell ◽  
Erk Signaling ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth

Cellular communication network factor 2 (CCN2, also known as CTGF), is a modular and matricellular protein and a well-known angiogenic factor in physiological and pathological angiogenesis. However, its roles in lymphangiogenesis and intracellular signaling in lymphatic endothelial cells (LECs) remain unclear. Here, we investigated CCN2 signaling in LECs and its effects on lymphangiogenesis. In primary cultured LECs, gene expressions of lymphatic endothelial markers lymphatic vessel endothelial hyaluronan receptor 1 (Lyve1), Podoplanin and prospero homeobox 1 (Prox1) and lymphangiogenic factors vascular endothelial cell growth factor c (Vegfc), vascular endothelial cell growth factor d (Vegfd) and fms-related tyrosine kinase 4 (Flt4, also known as Vegfr3) were upregulated by CCN2. Subsequently, we found that CCN2 induced phospho-ERK and that was decreased by suppression of integrin v. CCN2 slightly decreased the growth of LECs due to enhancement of the interaction of ERK and dual specific protein phosphatase 6 (DUSP6), and knockdown of DUSP6 increased CCN2-induced phospho-ERK levels. In in vivo Matrigel plug assays, the number of Podoplanin-positive vessels was increased by exogenous CCN2, and phospho-ERK-positive LEC and DUSP6-positive LEC were detected in CCN2 plugs. These results suggest that CCN2-related lymphangiogenesis is regulated by DUSP6, which enables negative modulation of ERK-signaling.

Platelet-derived endothelial cell growth factor mediates angiogenesis and antiapoptosis in rat aortic endothelial cells

2009 ◽  
Vol 87 (6) ◽  
pp. 883-893 ◽  
Author(s):  
Thiagarajan Hemalatha ◽  
Mitali Tiwari ◽  
Chidambaram Balachandran ◽  
Bhakthavatsalam Murali Manohar ◽  
Rengarajulu Puvanakrishnan
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Hypoxic Stress ◽  
Tubule Formation ◽  
Aortic Endothelial Cells ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth ◽  
Aortic Endothelial

This study explores the angiogenic and antiapoptotic activities of platelet-derived endothelial cell growth factor (PDECGF) in rat aortic endothelial cells. The effects of PDECGF on rat aortic endothelial cell (RAEC) proliferation, migration, chemotaxis, and tubule formation were investigated in vitro at various concentrations viz., 1, 2, 4, 8, 16, and 32 ng·mL–1 on endothelial cells. Endothelial cells were induced with hypoxic stress and the antiapoptotic effects of PDECGF were analysed by cell survival assay, fluorescence microscopy, cell viability assay, and flow cytometry. The results demonstrated the angiogenic potential of PDECGF on endothelial cells in a dose-dependent manner. PDECGF at 16 and 32 ng·mL–1 increased cell proliferation (>80%), induced cell migration (>4 fold), stimulated chemotaxis (>2 fold), and increased tubule formation (>3 fold) compared with the control. Studies on hypoxic stress revealed the antiapoptotic nature of PDECGF on endothelial cells. PDECGF treatment enhanced cell survival by 14%, as well as cell viability by 13%, and decreased the percentage of apoptotic cells by 13% as demonstrated by fluorescence-activated cell sorter studies (FACS). In conclusion, this study demonstrated the angiogenic and antiapoptotic potentials of PDECGF on RAEC.

scholarly journals Human endothelial cells are chemotactic to endothelial cell growth factor and heparin.

1985 ◽  
Vol 101 (6) ◽  
pp. 2330-2334 ◽  
Author(s):  
V P Terranova ◽  
R DiFlorio ◽  
R M Lyall ◽  
S Hic ◽  
R Friesel ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Migration ◽  
Growth Factors ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Endothelial Cell Migration ◽  
Human Endothelial Cells ◽  
Endothelial Cell Growth Factor ◽  
Endothelial Cell Growth

The response of human endothelial cell migration to various extracellular matrix components and growth factors has been assessed. Human endothelial cells demonstrate increased chemotaxis and chemokinesis when placed in a modified Boyden chamber with endothelial cell growth factor (ECGF) used at a concentration of 10(-9) M. Anti-ECGF antibody inhibits the chemotactic response. Heparin (10(-8) to 10(-10) M) was also chemotactic and was shown to potentiate the chemotactic activity of ECGF. Although laminin, fibronectin, the polypeptide (epidermal, fibroblast, and nerve) growth factors, and collagen types I, II, III, IV, and V demonstrate a chemotactic response, these activities were one third to one half less than observed with ECGF. These data suggest that ECGF and heparin may play a significant role as response modifiers of human endothelial cell migration which may be relevant to tumor metastasis, wound healing, and atherogenesis.

Vascular Endothelial Cell Growth Factor–Induced Tissue Factor Expression in Endothelial Cells Is Mediated by EGR-1

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3811-3823 ◽  
Author(s):  
Diana Mechtcheriakova ◽  
Alexander Wlachos ◽  
Harry Holzmüller ◽  
Bernd R. Binder ◽  
Erhard Hofer
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Tissue Factor ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Growth Factor ◽  
Inflammatory Stimuli ◽  
Endothelial Cell Growth

Abstract Vascular endothelial cell growth factor (VEGF) is a major regulator of angiogenesis. We report here that treatment of endothelial cells with VEGF leads to upregulation of tissue factor mRNA and protein expression on the cell surface. Reporter gene studies show that transcriptional activation of the tissue factor gene by VEGF is mediated by a GC-rich promoter element containing overlapping binding sites for Sp1 and EGR-1. As shown by immunofluorescence and electrophoretic mobility shift assays, upon VEGF treatment EGR-1 rapidly accumulates in the nucleus and binds to its respective recognition site in the tissue factor promoter. Sp1 occupies this element in unstimulated cells and seems to be partially displaced by increasing amounts of EGR-1. Transfection of endothelial cells with an EGR-1 expression plasmid mimics the upregulation of tissue factor transcription observed after VEGF treatment. In contrast, NFκB, the major transcription factor involved in tissue factor upregulation by inflammatory stimuli, is not activated by VEGF. These data show that VEGF induces a response in endothelial cells largely distinct from inflammatory stimuli, and suggest that EGR-1 is a major mediator of the activation of the tissue factor and possibly other VEGF-responsive genes.

Vascular Endothelial Cell Growth Factor–Induced Tissue Factor Expression in Endothelial Cells Is Mediated by EGR-1

Blood ◽  
1999 ◽  
Vol 93 (11) ◽  
pp. 3811-3823 ◽  
Author(s):  
Diana Mechtcheriakova ◽  
Alexander Wlachos ◽  
Harry Holzmüller ◽  
Bernd R. Binder ◽  
Erhard Hofer
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Cell Growth ◽  
Tissue Factor ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Growth Factor ◽  
Inflammatory Stimuli ◽  
Endothelial Cell Growth

Vascular endothelial cell growth factor (VEGF) is a major regulator of angiogenesis. We report here that treatment of endothelial cells with VEGF leads to upregulation of tissue factor mRNA and protein expression on the cell surface. Reporter gene studies show that transcriptional activation of the tissue factor gene by VEGF is mediated by a GC-rich promoter element containing overlapping binding sites for Sp1 and EGR-1. As shown by immunofluorescence and electrophoretic mobility shift assays, upon VEGF treatment EGR-1 rapidly accumulates in the nucleus and binds to its respective recognition site in the tissue factor promoter. Sp1 occupies this element in unstimulated cells and seems to be partially displaced by increasing amounts of EGR-1. Transfection of endothelial cells with an EGR-1 expression plasmid mimics the upregulation of tissue factor transcription observed after VEGF treatment. In contrast, NFκB, the major transcription factor involved in tissue factor upregulation by inflammatory stimuli, is not activated by VEGF. These data show that VEGF induces a response in endothelial cells largely distinct from inflammatory stimuli, and suggest that EGR-1 is a major mediator of the activation of the tissue factor and possibly other VEGF-responsive genes.

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