Stimulation of Growth and Migration of Vascular Endothelial Cells by Vascular Endothelial Growth Factor Transduced Smooth Muscle Cells in Co-Culture

ASAIO Journal ◽  
1997 ◽  
Vol 43 (5) ◽  
pp. M759 ◽  
Author(s):  
PRIYA VISWESWARAN ◽  
A. DANIEL JOHNSON ◽  
CHRISTINE L. TOCK ◽  
DAVID A. EMGLER ◽  
JOHN J. SCHWARZ ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
And Migration ◽  
Endothelial Growth Factor ◽  
Stimulation Of

scholarly journals Nitric oxide mediates the mitogenic effects of insulin and vascular endothelial growth factor but not of leptin in endothelial cells.

1999 ◽  
Vol 46 (3) ◽  
pp. 703-715 ◽  
Author(s):  
A Józkowicz ◽  
J Pankiewicz ◽  
J Dulak ◽  
L Partyka ◽  
I Wybrańska ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Vegf Protein

The regulation of vascular wall homeostasis by nitric oxide (NO) generated by endothelium is being intensively studied. In the present paper, the involvement of NO in the vascular endothelial growth factor (VEGF), insulin or leptin-stimulated proliferation of human endothelial cells (HUVEC) was measured by [3H]thymidine or bromodeoxyuridine incorporation. VEGF and insulin, but not leptin, increased NO generation in HUVEC, as detected with ISO-NO electrode. Proliferation of HUVEC induced by leptin was not changed or was higher in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) a nitric oxide synthase (NOS) inhibitor. In contrast, L-NAME blunted the proproliferative effect of VEGF and insulin. Furthermore, we demonstrated that, in human arterial smooth muscle cells (hASMC) transfected with endothelial NOS (eNOS) gene, the generation of biologically active VEGF protein was NO-dependent. Inhibition of NO generation by L-NAME decreased the synthesis of VEGF protein and attenuated HUVEC proliferation induced by conditioned media from transfected hASMC. Endothelium-derived NO seems to participate in VEGF and insulin, but not leptin, mitogenic activity. Additionally, the small amounts of NO released from endothelial cells, as mimicked by eNOS transfection into hASMC, may activate generation of VEGF in sub-endothelial smooth muscle cells, leading to increased synthesis of VEGF protein necessary for turnover and restitution of endothelial cells.

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