Visfatin promotes angiogenesis by activation of extracellular signal-regulated kinase 1/2 |
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Authors: | Kim Su-Ryun Bae Soo-Kyung Choi Kyu-Sil Park Shi-Young Jun Hyung Oh Lee Ju-Youn Jang Hye-Ock Yun Il Yoon Kwon-Ha Kim Yung-Jin Yoo Mi-Ae Kim Kyu-Won Bae Moon-Kyoung |
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Institution: | School of Dentistry, Pusan National University, Pusan 602-739, Republic of Korea. |
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Abstract: | Adipose tissue is highly vascularized and requires the angiogenic properties for its mass growth. Visfatin has been recently characterized as a novel adipokine, which is preferentially produced by adipose tissue. In this study, we report that visfatin potently stimulates in vivo neovascularization in chick chorioallantoic membrane and mouse Matrigel plug. We also demonstrate that visfatin activates migration, invasion, and tube formation in human umbilical vein endothelial cells (HUVECs). Moreover, visfatin evokes activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) in endothelial cells, which is closely linked to angiogenesis. Inhibition of ERK activation markedly decreases visfatin-induced tube formation of HUVECs and visfatin-stimulated endothelial cell sprouting from rat aortic rings. Taken together, these results demonstrate that visfatin promotes angiogenesis via activation of mitogen-activated protein kinase ERK-dependent pathway and suggest that visfatin may play important roles in various pathophysiological angiogenesis including adipose tissue angiogenesis. |
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Keywords: | Visfatin Vascular endothelial cells Angiogenesis ERK |
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