The effects of oxLDL on SOD or catalase-transfected human aortic endothelial cells

碩士 === 國立陽明大學 === 解剖暨細胞生物學研究所 === 90 === Reactive oxygen metabolites such as superoxide ions (O2.—)and hydrogen peroxide (H2O2) are proinflammatory and are involved in the pathophysiology of various diseases including atherosclerosis. To determine whether the intracellular superoxide dism...

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Bibliographic Details
Main Authors: Po-Len Liu, 劉博侖
Other Authors: Yuh-Lien Chen
Format: Others
Language:zh-TW
Published: 2002
Online Access:http://ndltd.ncl.edu.tw/handle/75591022623765732563
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Summary:碩士 === 國立陽明大學 === 解剖暨細胞生物學研究所 === 90 === Reactive oxygen metabolites such as superoxide ions (O2.—)and hydrogen peroxide (H2O2) are proinflammatory and are involved in the pathophysiology of various diseases including atherosclerosis. To determine whether the intracellular superoxide dismutase (SOD) and catalase (CAT) have a protective effect, human aortic endothelial cells (HAECs) were transfected with adenoviral vector containing cDNA for human Cu/ZnSOD (AdSOD) or catalase (AdCAT). Adenoviral transfection increased the content and activity of SOD or catalase in the cells. HAECs transfected with AdSOD and AdCAT decreased superoxide ions and hydrogen peroxide production in oxLDL-treated HAECs, respectively. AdSOD or AdCAT transfection also inhibited oxLDL-induced cell apoptosis. To explore the transcriptional effects of catalase overexpression in oxLDL-induced HAECs apoptosis was used by cDNA array. Gene expression analysis showed that several apoptosis-related genes such as TNFR, Bcl-2 like 11, X-linked IAP, FADD, apoptosis regulator (bar), TRAF-4, caspase-3, caspase-9, etc. were regulated by oxLDL treatment. Gene transfer with catalase led to significant inhibition of JNK, AP-1, ERK expression in oxLDLD treated HAECs, while the expressions of NF-kB and p38 were not altered. These results suggest that transferring catalase gene will increase cellular viability via inhibiting the pro-apoptotic activation of JNK/AP-1 pathway and promoting the expression of some anti-apoptotic proteins, such as ERK and Bcl-2.