國家衛生研究院 NHRI:Item 3990099045/1454
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    題名: Shear stress regulates gene expression in vascular endothelial cells in response to tumor necrosis factor-alpha: A study of the transcription profile with complementary DNA microarray
    作者: Chiu, JJ;Lee, PL;Chang, SF;Chen, LJ;Lee, CI;Lin, KM;Usami, S;Chien, S
    貢獻者: Division of Medical Engineering Research
    摘要: We investigate the role of shear stress in regulating the gene expression in endothelial cells (ECs) in response to tumor necrosis factor-alpha (TNF-alpha). ECs were kept in static condition or pre- exposed to a high level (HSS, 20 dynes/cm(2)) or a low level of shear stress (LSS, 0.5 dynes/cm(2)) for 24 h, and TNF-alpha was added under static condition for 4 h. In static ECs, DNA microarray showed that TNF-alpha caused a significant increase in expression of 102 genes and a significant decrease in expression of 12 genes. Pre-shearing of ECs decreased the TNF-alpha-responsiveness of many pro-inflammatory, pro-coagulant, proliferative, and pro-apoptotic genes, whereas it increased the responsiveness of some antioxidant, anti- coagulant, and anti- apoptotic genes. LSS showed less regulatory effects than HSS on EC gene expression in response to TNF-alpha. The microarray data were confirmed by reverse-transcription polymerase chain reaction for 64 selected genes. Pre-shearing of ECs at HSS significantly inhibited the TNF-alpha-induced p65 and p50 mRNA expressions and nuclear factor-kappa B (NF-kappa B)-DNA binding activity. Inhibition of NF-kappa B activity with the p65-antisense or lactacystin under static condition blocked the expression of most of the genes that are TNF-alpha-inducible and shear stress-down-regulated. Our findings suggest that laminar shear stress serves protective functions against atherogenesis.
    關鍵詞: Medicine, Research & Experimental
    日期: 2005-05
    關聯: Journal of Biomedical Science. 2005 May;12(3):481-502.
    Link to: http://dx.doi.org/10.1007/s11373-005-4338-4
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1021-7770&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000230695300005
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=22744459308
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