scholarly journals Azelnidipine, Not Amlodipine, Induces Secretion of Vascular Endothelial Growth Factor From Smooth Muscle Cells and Promotes Endothelial Tube Formation

2014 ◽  
Vol 5 (5) ◽  
pp. 145-150 ◽  
Author(s):  
Akira Kawamura ◽  
Shin-ichiro Miura ◽  
Yoshino Matsuo ◽  
Hiroyuki Tanigawa ◽  
Keijiro Saku
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tube Formation ◽  
Vascular Endothelial ◽  
Endothelial Tube Formation ◽  
Endothelial Growth Factor

Vascular Endothelial Growth Factor-Induced Migration of Vascular Smooth Muscle Cells in Vitro

1999 ◽  
Vol 58 (2) ◽  
pp. 128-136 ◽  
Author(s):  
Cynthia L. Grosskreutz ◽  
Bela Anand-Apte ◽  
Cécile Dupláa ◽  
Timothy P. Quinn ◽  
Bruce I. Terman ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

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.

scholarly journals Ligands of peroxisome proliferator-activated receptor-gamma increase the generation of vascular endothelial growth factor in vascular smooth muscle cells and in macrophages.

2000 ◽  
Vol 47 (4) ◽  
pp. 1147-1157 ◽  
Author(s):  
A Jozkowicz ◽  
J Dulak ◽  
E Piatkowska ◽  
W Placha ◽  
A Dembinska-Kiec
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Peroxisome Proliferator ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Peroxisome proliferator-activated receptors-gamma (PPARgamma) are ligand-inducible transcription factors of the nuclear hormone receptor superfamily. We examined the effect of PPARgamma activation on the generation of vascular endothelial growth factor (VEGF), one of the major angiogenic agents. Rat vascular smooth muscle cells (VSMC) and murine macrophages RAW264.7 were incubated for 24 h with PPARgamma activators: prostaglandin J2 and ciglitazone. PPARgamma were expressed in VSMC and RAW cells and their activity was upregulated in the presence of PGJ2 and ciglitazone. Incubation of the cells with PPARgamma activators significantly augmented the release of VEGF protein into the media, both in resting and in IL-1beta- or LPS-stimulated cultures. The higher protein generation was connected with the increased expression of mRNA and transcriptional activation of VEGF promoter. We conclude that the activation of PPARgamma upregulates the generation of VEGF and may be involved in the regulation of angiogenesis.

Sign in / Sign up

Export Citation Format

Share Document