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    題名: Prognostic value of p53 expression in stage IB1 cervical carcinoma
    作者: Chen, HY;Hsu, CT;Lin, WC;Tsai, HD;Chang, WC
    貢獻者: 附設醫院婦產部;China Med Coll Hosp, Dept Obstet & Gynecol, Taichung, Taiwan;China Med Coll Hosp, Dept Pathol, Taichung, Taiwan;China Med Coll, Inst Med Sci, Taichung, Taiwan
    日期: 2000
    上傳時間: 2010-09-24 14:47:44 (UTC+8)
    出版者: KARGER
    摘要: Background-Diabetes mellitus causes multiple cardiovascular complications. High glucose can induce reactive oxygen species and apoptosis in endothelial cells. Little is known about the molecular mechanisms in high glucose-induced endothelial cell apoptosis. Methods and Results-We elucidated the signaling pathway of high glucose-induced apoptosis in human umbilical vein endothelial cells (HUVECs). HUVECs were treated with media containing 5.5, 19, or 33 mmol/L of glucose in the presence or absence of an antioxidant, ascorbic acid. The level of intracellular H2O2 was measured by flow cytometry. For detection of apoptosis, the cell death detection ELISA assay and the morphological Hoechst staining were used. High glucose was capable of inducing the activity of c-Jun NH2-terminal kinase (JNK) but not extracellular signal-regulated kinase 1/2 or p38 mitogen-activated protein kinase during the treatment periods, as evidenced by immunocomplex kinase assay. Moreover, we found that the interleukin 1 beta-converting enzyme (ICE)/CED-3 family protease (caspase-3) became activated in high glucose-induced apoptosis. Caspase-3/CPP32-specific inhibitor, Ac-DEVD-CHO, could inhibit high glucose-induced apoptosis. Furthermore, we found that JNK1 specific antisense oligonucleotide could suppress caspase-3 activity but not affect H2O2 generation and could block apoptosis induced by high glucose. Also, H2O2 generation, JNK activity, caspase-3 activity, and the subsequent apoptosis induced by high glucose could be suppressed by ascorbic acid. Conclusions-The present study indicates that reactive oxygen species induced by high glucose may be involved in JNK activation, which in turn triggers the caspase-3 that facilitates the apoptosis in HUVECs.
    關聯: GYNECOLOGIC AND OBSTETRIC INVESTIGATION 49(4):266-271
    顯示於類別:[台中附設醫院] 期刊論文

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