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Effects of 15-deoxy-Δ~(12,14)-prostaglandin J_2 on cell proliferation and apoptosis in ECV304 endothelial cells

机译:15-脱氧-Δ〜(12,14)-前列腺素J_2对ECV304内皮细胞增殖和凋亡的影响

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AIM: To investigate the effects of 15-deoxy-Δ~(12,14)-prostaglandin J_2 (15d-PGJ_2) on cell proliferation and apoptosis in ECV304 endothelial cells and related molecular mechanism. METHODS: MTT, Hoechst33258, TUNEL, Flow cytometry, DNA ladder, RT-PCR, Western blot, and electrophoretic mobility shift assay (EMSA) analysis were employed. RESULTS: The 15d-PGJ_2 induced apoptosis in ECV304 endothelial cells in a dose-dependent manner (the percentage of apoptosis was enhanced from 10.0 %+-1.3 % to 32.8 %+-1.6 %), which was accompanied by inhibition of NF-κB and AP-1 DNA binding activity, down-regulation of c-myc, upregulation of Gadd45 and p53, and activation of p38 kinase. However, the expression of p21 was found no significant change. CONCLUSION: peroxisome proliferator-activated receptor gamma ligand, 15d-PGJ_2, can inhibit proliferation and induce apoptosis in ECV304 endothelial cells through different mechanisms.
机译:目的:研究15-脱氧-Δ〜(12,14)-前列腺素J_2(15d-PGJ_2)对ECV304内皮细胞增殖和凋亡的影响及其分子机制。方法:采用MTT,Hoechst33258,TUNEL,流式细胞仪,DNA阶梯,RT-PCR,Western印迹和电泳迁移率变动分析(EMSA)分析。结果:15d-PGJ_2诱导ECV304内皮细胞凋亡呈剂量依赖性(凋亡百分比从10.0%+-1.3%增加到32.8%+ -1.6%),并伴有NF-κB的抑制作用和AP-1 DNA结合活性,c-myc的下调,Gadd45和p53的上调以及p38激酶的激活。然而,发现p21的表达没有明显变化。结论:过氧化物酶体增殖物激活受体γ配体15d-PGJ_2可以通过不同机制抑制ECV304内皮细胞的增殖并诱导其凋亡。

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