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Please use this identifier to cite or link to this item:
https://ir.csmu.edu.tw:8080/ir/handle/310902500/4409
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Title: | Helicobacter pylori-derived Heat shock protein 60 enhances angiogenesis via a CXCR2-mediated signaling pathway |
Authors: | Lina, Chen-Si Hea, Pei-Juin Hsua, Wei-Tung Wuc, Ming-Shiang Wud, Chang-Jer Shene, Hsiao-Wei Hwangg, Chia-Hsiang Laif, Yiu-Kay Tsaih, Nu-Man Liaoe, Kuang-Wen |
Contributors: | 中山醫學大學 醫學檢驗暨生物技術學系 |
Keywords: | Helicobacter pylori Heat shock protein 60 CXCR2 Angiogenesis |
Date: | 2010-05-24 |
Issue Date: | 2012-08-06T09:08:37Z (UTC)
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ISSN: | 0006-291X |
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 PLCβ2/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/PLCβ2/Ca2+ signal transduction in endothelial cells. |
URI: | https://ir.csmu.edu.tw:8080/ir/handle/310902500/4409 http://dx.doi.org/10.1016/j.bbrc.2010.05.101 |
Relation: | Biochemical and Biophysical Research Communications Volume 397, Issue 2, 25 June 2010, Pages 283–289 |
Appears in Collections: | [醫學檢驗暨生物技術學系暨碩士班] 期刊論文
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