内源性TGF—β1、TNF—α在三氧化二砷诱导HL—60细胞凋亡中作用的研究 |
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作者单位: | 陈元仲(350001,福州,福建省血液病研究所,福建医科大学附属协和医院);吴勇(350001,福州,福建省血液病研究所,福建医科大学附属协和医院);黄美娟(350001,福州,福建省血液病研究所,福建医科大学附属协和医院);吕联煌(350001,福州,福建省血液病研究所,福建医科大学附属协和医院) |
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基金项目: | 国家教委优秀年轻教师基金资助项目(95-503);福建省教委科研基金资助项目(K95033);国家"百千万人才工程"专项基金资助项目 |
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摘 要: | 目的探讨内源性TGF-β
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关 键 词: | 白血病 HL-60细胞 细胞凋亡 三氧化二砷 内源性转化生长因子-β1 肿瘤坏死因子-α bcl-2 反义磷酸硫代脱氧寡核酸 |
修稿时间: | 2002年8月12日 |
Effect of endogenous TGF- |
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Authors: | Yuan-zhong Chen Yong Wu Mei-juan Huang Lian-huang Lu |
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Institution: | Fujian Institute of Hematology, Union Hospital, Fujian Medical University, Fuzhou 350001, China. |
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Abstract: | OBJECTIVE: To study the effect of endogenous TGF-beta(1) and TNF-alpha on As(2)O(3) inducing apoptosis of HL-60 cells. METHODS: The expressions of endogenous TGF-beta(1) and TNF-alpha in apoptotic HL-60 cells induced by As(2)O(3) were assayed by RT-PCR, quantitative RT-PCR, ELISA, DNA fragmentation and TUNEL. The effect of TGF-beta(1) and TNF-alpha antisense phosphorothioate oligodeoxynucleotides (PSODNs) on As(2)O(3) inducing apoptotic HL-60 cells was further studied. RESULTS: (1) Expressions of endogenous TGF-beta(1) and TNF-alpha were significantly up-regulated in As(2)O(3) inducing apoptotic HL-60 cells (from 13,546 +/- 124 and 497,216 +/- 187 before treatment to 23,273 +/- 229 and 674,217 +/- 189 after treatment, respectively), accompanied with down-regulated bcl-2 mRNA expression (from 10,424 +/- 274 before treatment to 3,361 +/- 89 after treatment). (2) TGF-beta(1) and TNF-alpha antisense PSODNs could rescue As(2)O(3) induced apoptosis of HL-60 cells, with a restoration of bcl-2 gene expression. CONCLUSIONS: Endogenous TGF-beta(1) and TNF-alpha played an important role in As(2)O(3) inducing HL-60 cells apoptosis through down-regulation of bcl-2 expression. |
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