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題 名 | Molecular Mechanisms in Peptidoglycan-Induced Human Umbilical Vascular Endothelial Cell Apoptosis=肽聚醣誘導人類臍靜脈內皮細胞凋亡之機轉 |
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作 者 | 張藏能; 邱佩婷; 陳威銓; 許銘仁; | 書刊名 | Journal of Food and Drug Analysis |
卷 期 | 19:2 2011.06[民100.06] |
頁 次 | 頁159-166+240 |
分類號 | 415.27 |
關鍵詞 | 敗血症; 血管滲漏症狀; 肽聚醣; 革蘭氏陽性菌; Sepsis; Vascular leak syndromes; Peptidoglycan; PGN; ASK1; Apoptosis signal regulating kinase 1; |
語 文 | 英文(English) |
英文摘要 | Peptidoglycan (PGN), a component of the outer membrane of Gram-positive bacteria has been implicated in the pathological process of sepsis. However, the molecular mechanism of PGN-induced vascular endothelium dysfunction has not been fully elucidated. Apoptosis signal regulating kinase 1 (ASK1) has been recently reported to play a crucial role in cell apoptosis under various cellular stresses. The purpose of this study was thus to investigate whether PGN-activated ASK1 results in cell apoptosis in human umbilical vascular endothelial cells (HUVECs). PGN was shown to cause a decrease in cell viability in a concentration-dependent manner. Flow cytometric analysis demonstrated that PGN increased the percentage of apoptotic cells. PGN induced ASK1 activation was accompanied by the increased phosphorylation of p38MAPK, a major downstream signaling molecule of ASK1. In addition, PGN was shown to increase apoptotic protein, Bax, expression in HUVECs. Inhibitor of p38MAPK signaling abrogated the PGN-increased DNA fragmentation and Bax expression, suggesting functional crosstalk. The toll-like receptor 2 (TLR2) agonist, Pam3CSK4, was also shown to induce ASK1 activation and p38MAPK phosphorylation, and subsequent cell apoptosis in HUVECs. Our data suggest that ASK1-p38MAPK cascade activation, followed by Bax expression, contributes to PGN-induced cell apoptosis. |
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