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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/18814
Title: Induction of high mobility group box 1 release from serotonin-stimulated human umbilical vein endothelial cells
Authors: Ko Ichi Kawahara
Teruto Hashiguchi
Kiyoshi Kikuchi
Salunya Tancharoen
Naoki Miura
Takashi Ito
Yoko Oyama
Yuko Nawa
Kamal K. Biswas
Xiaojie Meng
Yoko Morimoto
Binita Shrestha
Hisayo Sameshima
Ikuro Maruyama
Kagoshima University Faculty of Medicine
Mahidol University
Kagoshima University
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Dec-2008
Citation: International Journal of Molecular Medicine. Vol.22, No.5 (2008), 639-644
Abstract: High mobility group box 1 (HMGB1) is a nonhistone nuclear protein which is released from the nucleus of activated macrophages into the extracellular space in response to stimuli such as endotoxin or necrosis. The HMGB1 functions as a potent proinflammatory cytokine in the extracellular spaces. Recently, HMGB1 has been implicated in the progression of atherosclerosis. However, the association between HMGB1 and the development of atherosclerosis is poorly understood. Therefore, we examined whether serotonin (5-HT), a key factor involved in the development of atherosclerosis, induced HMGB1 release in human umbilical vein endothelial cells (HUVECs). We found that 5-HT induced the release of HMGB1 but not of ERK1/2 and JNK from HUVECs via the 5-HT receptor (5-HT1B)/p38 mitogen-activated protein kinase (MAPK) signaling pathway. The p38MAPK inhibitor SB203580 and the 5-HT1B antagonist GR55526 markedly inhibited HMGB1 release from 5-HT-stimulated HUVECs. The vascular endothelial growth factor (VEGF) derived from activated macrophages in atherosclerotic lesions also plays an important role in the progression of atherosclerosis. We found that HMGB1 induced VEGF production in macrophage-like RAW264.7 cells. HMGB1 induced the activation of p38MAPK, ERK1/2 and Akt. The PI3-kinase inhibitor LY294002 significantly inhibited VEGF production in HMGB1-stimulated macrophages, while other kinase inhibitors did not. These results suggest that HMGB1 release may contribute as a risk factor in the development and progression of atherosclerosis.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=59149099449&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/18814
ISSN: 1791244X
11073756
Appears in Collections:Scopus 2006-2010

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