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Ascites from cirrhotic patients induces angiogenesis through the phosphoinositide 3-kinase/Akt signaling pathway.

Abstract：

BACKGROUND/AIMS:Ascites in patients with cirrhosis is associated with worsening of systemic hemodynamics. Thus, the aim of this study was to investigate the biological activity of ascites on endothelial cells. METHODS:Human umbilical vein endothelial cells (HUVECs) were used to investigate the angiogenic activity of ascites obtained from cirrhotic patients. RESULTS:Ascites-induced Akt activation, cell migration and tube formation in HUVECs. The pretreatment of HUVECs with the phosphatidylinositide 3-kinase (PI3-kinase) inhibitor LY294002, resulted in a decrease in chemotaxis and cell tube formation induced by ascites. Moreover, the inhibition of Akt activity in HUVECs by transduction of an inactive phosphorylation Akt mutant (AA-Akt), blocked tube formation. These angiogenic effects of ascites were also operative in vivo showing a PI3-kinase activation dependence in the angiogenesis induced by ascites. In addition, the preincubation of ascites with anti-fibronectin antibody led to a significant decrease in HUVECs migration, cell tube formation and in vivo angiogenesis. CONCLUSIONS:These results confirm the novel concept that ascites is a bioactive fluid which can modify vascular properties through the activation of the PI3-kinase/Akt pathway in endothelial cells. Furthermore, our results demonstrated that this ascites-induced mechanism is mediated, at least in part, by fibronectin.

journal_name

J Hepatol

journal_title

Journal of hepatology

authors

Morales-Ruiz M,Tugues S,Cejudo-Martín P,Ros J,Melgar-Lesmes P,Fernández-Llama P,Arroyo V,Rodés J,Jiménez W

doi

10.1016/j.jhep.2005.01.035

subject

Has Abstract

pub_date

2005-07-01 00:00:00

pages

85-91

issue

1

eissn

0168-8278

issn

1600-0641

pii

S0168-8278(05)00204-7

journal_volume

43

pub_type

杂志文章

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