Title: Helicobacter pylori-derived Heat shock protein 60 enhances angiogenesis via a CXCR2-mediated signaling pathway
Authors: Lin, Chen-Si
He, Pei-Juin
Hsu, Wei-Tung
Wu, Ming-Shiang
Wu, Chang-Jer
Shen, Hsiao-Wei
Hwang, Chia-Hsiang
Lai, Yiu-Kay
Tsai, Nu-Man
Liao, Kuang-Wen
Institute of Molecular Medicine and Bioengineering
Keywords: Helicobacter pylori;Heat shock protein 60;Angiogenesis;CXCR2
Issue Date: 25-Jun-2010
Abstract: Helicobacter pylori is a potent carcinogen associated with gastric cancer malignancy. Recently. H. pylori Heat shock protein 60 (HpHSP60) has been reported to promote cancer development by inducing chronic inflammation and promoting tumor cell migration. This study demonstrates a role for HpHSP60 in angiogenesis, a necessary precursor to tumor growth. We showed that HpHSP60 enhanced cell migration and tube formation, but not cell proliferation, in human umbilical vein endothelial cells (HUVECs). HpHSP60 also indirectly promoted HUVEC proliferation when HUVECs were co-cultured with supernatants collected from HpHSP60-treated AGS or THP-1 cells. The angiogenic array showed that HpHSP60 dramatically induced THP-1 cells and HUVECs to produce the chemotactic factors IL-8 and GRO. Inhibition of CXCR2, the receptor for IL-8 and GRO, or downstream PLC beta 2/Ca2+-mediated signaling, significantly abolished HpHSP60-induced tube formation. In contrast, suppression of MAP K or PI3 K signaling did not affect HpHSP60-mediated tubulogenesis. These data suggest that HpHSP60 enhances angiogenesis via CXCR2/PLC beta 2/Ca2+ signal transduction in endothelial cells. (C) 2010 Elsevier Inc. All rights reserved.
URI: http://dx.doi.org/10.1016/j.bbrc.2010.05.101
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2010.05.101
Volume: 397
Issue: 2
Begin Page: 283
End Page: 289
Appears in Collections:Articles

Files in This Item:

  1. 000279718900028.pdf