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Upregulation of fibroblast growth factor-2 by visfatin that promotes endothelial angiogenesis. | LitMetric

Upregulation of fibroblast growth factor-2 by visfatin that promotes endothelial angiogenesis.

Biochem Biophys Res Commun

Department of Physiology, School of Medicine, Pusan National University, Busan 602-739, South Korea.

Published: February 2009

AI Article Synopsis

  • Adipokines, specifically visfatin, play a role in regulating angiogenesis, which is the formation of new blood vessels.
  • This study reveals that visfatin promotes angiogenesis through the activation of fibroblast growth factor-2 (FGF-2) in human endothelial cells, enhancing both FGF-2 mRNA and protein levels.
  • The process is dependent on the extracellular signal-regulated kinase 1/2 (Erk1/2) pathway and involves two main steps: visfatin-induced expression of FGF-2 and subsequent FGF-2-driven angiogenesis.

Article Abstract

Adipokines have been known to act as angiogenic regulators in the process of angiogenesis. Recently, we have demonstrated that visfatin, a novel adipokine, has angiogenic activity. However, little has been reported on the underlying mechanism of visfatin-induced angiogenesis. In this study, we report that visfatin-induced angiogenesis is mediated by endothelial fibroblast growth factor-2 (FGF-2). Visfatin increased the levels of FGF-2 mRNA and protein in human endothelial cells. The enhancement in FGF-2 expression was prevented by an inhibitor of the extracellular signal-regulated kinase 1/2 (Erk1/2) pathway. Furthermore, visfatin-induced angiogenesis was reduced by inhibition of FGF-2 receptor kinase or by neutralization of FGF-2 function. Taken together, our results indicate that visfatin-induced endothelial angiogenesis is composed largely of two sequential steps: the induction of Erk1/2-dependent FGF-2 gene expression by visfatin and the subsequent FGF-2-induced angiogenesis. These data further suggest an integral role for visfatin-FGF-2 signaling axis in modulating endothelial angiogenesis.

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Source
http://dx.doi.org/10.1016/j.bbrc.2008.12.042DOI Listing

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