Vasostatin Inhibits VEGF-Induced Endothelial Cell Proliferation, Tube Formation and Induces Cell Apoptosis under Oxygen Deprivation

International Journal of Molecular Sciences

Qun Shu¹  Wenjiao Li¹  Haichuan Li¹ 

[1] Shanghai Changning Maternity and Infant Health Hospital, 773 Wuyi Road, Shanghai 200051, China; E-Mails:

关键词: vasostatin;    human umbilical vein endothelial cells (HUVEC);    angiogenesis;    mitochondrial apoptosis;   

DOI  :  10.3390/ijms15046019

来源: mdpi

【 摘 要 】

Anti-angiogenesis treatment has been a promising new form of cancer therapy. Endothelial cells are critical for vascular homeostasis and play important roles in angiogenesis, vascular and tissue remodeling. Vasostatin, the 180 amino acid N-terminal fragment of the calreticulin protein, is reported to be a potent endogenous inhibitor of angiogenesis, suppressing tumor growth. However, the mechanism of these effects has not been sufficiently investigated. This study was performed to investigate the possible mechanism of vasostatin effects on primary cultured human umbilical vein endothelial cells (HUVEC). We found that vasostatin could inhibit the cell viability of HUVEC and induce cell apoptosis through mitochondrial pathways via activation of caspase-3 under oxygen deprivation conditions. Meanwhile, vasostatin also inhibited vascular endothelial growth factor-induced proliferation and tube formation of HUVEC. The possible mechanism of vasostatin-inhibited proliferation of HUVEC could be through down-regulation of endothelial nitric oxide synthase. These findings suggest that vasostatin could regulate endothelial cell function and might be used in anti-angiogenesis treatment.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland