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題 名 | Shear Stress Attenuates Tumor Necrosis Factor-广-Induced Monocyte Chemotactic Protein-1 Expressions in Endothelial Cells |
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作 者 | Chiu,Jeng-jiann; Lee,Pei-ling; Lee,Chih-i; Chen,Li-jing; Chen,Cheng-nan; Ko,Ya-chen; Lien,Sheng-chieh; | 書刊名 | 中國生理學雜誌 |
卷 期 | 45:4 2002.12[民91.12] |
頁 次 | 頁169-176 |
分類號 | 415.13 |
關鍵詞 | Endothelial cell; Cytokine; Monocyte chemotactic protein; Shear stress; |
語 文 | 英文(English) |
英文摘要 | The interplay between shear stress and cytokines in regulating vascular endothelial function remains largely unexplored. In the present study, the potential role of shear stress in regulating tumor necrosis factor-α (TNF-α)-induced gene expression in endothelial cells(ECs)was investigated. The TNF-α-induced monocyte chemotactic protein-1(MCP-1)mRNA expressions were significantly attenuated in ECs subjected to a high level of shear stress(20 dynes/cm²) for 4 or 24 h prior to the addition of TNF-α in the presence of flow. Less inhibition of TNF-α-induced MCP-1 mRNA expression was found in ECs pre-exposed to a low level of shear stress(1.2 dynes/cm²) for 24 h as compared with the cells presheared(pre-exposed to shear stress) for 4 h. Simultaneous exposure of ECs to TNF-α and a high or low level of shear stress down-regulated TNF-α-induced MCP-1 gene expressions, suggesting that the post-flow condition modulates endothelial responses to cytokine stimulation. Individually or combined, an endothelial nitric oxide synthase (eNOS) inhibitor and a glutathione(GSH) biosynthesis inhibitor had no effect on this shear stress-mediated inhibition. Moreover, in ECs either presheared or remained in a static condition prior to stimulation by TNF-α while under shear flow, the ability of TNF-α to induce AP-1-DNA binding activity in the nucleus was reduced. Our findings suggest that shear stress plays a protective role in vascular homeostasis by inhibiting endothelial responses to cytokine stimulation. |
本系統中英文摘要資訊取自各篇刊載內容。