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Parathyroid hormone stimulates the endothelial expression of vascular endothelial growth factor

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ABSTRACT Background 

We showed previously that parathyroid hormone (PTH) may stimulate the endothelial expression of pro-atherosclerotic and pro-inflammatory markers. Considering the impact of PTH on vasculature, we decided to evaluate its effect on mRNA and intra-cellular protein expressions of endothelial vascular endothelial growth factor (VEGF) taking into account that VEGF may play a role in the pathogenesis of endothelial dysfunctions. Materials and methods 

Human umbilical vein cords endothelial cells (HUVEC) were stimulated for 24 h with 10−12–10−10 mol L−1 PTH. The VEGF-165 mRNA expression (critical in stimulating endothelial cell proliferation) was evaluated by RT/PCR and the intra-cellular VEGF protein expression by flow cytometry. The pathways by which PTH may have an effect on VEGF expression were also evaluated. Results 

PTH (10−10 mol L−1) significantly increased VEGF-165 mRNA expression (P < 0·05). The addition of 50 nmol L−1 protein kinase C (PKC) and 10 µmol L−1 protein kinase A (PKA) inhibitors significantly reduced the VEGF-165 mRNA expression (P = 0·01). We also examined whether nitric oxide (NO) may be involved in the PTH-induced stimulation of VEGF-165 expression. Pre-treatment of the cells with 200 µmol L-nitro arginine methyl ester (L-NAME, NO synthase inhibitor) was found to inhibit VEGF-165 mRNA expression (P = 0·006). VEGF protein could not be detected in the medium of HUVEC but it was present in the cell cytoplasm. PTH had no significant effect on cytoplasmatic VEGF protein expression. Conclusion 

The stimulatory effect of PTH on endothelial VEGF-165 mRNA expression is partly through PKC and PKA pathways and is also NO dependent.

Eur J Clin Invest 2008; 38 (11): 798–803

Keywords: Endothelial cells; PKA; PKC; PTH; VEGF

Document Type: Research Article


Affiliations: Renal Physiology Laboratory, Department of Nephrology and Hypertension, Meir Medical Center, Kfar-Saba and

Publication date: November 1, 2008


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