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细胞因子对小鼠 2 I 型前胶原基因启动子活性影响的研究 |
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高春芳 印 彤 王 皓 孔宪涛
中国图书分类号 R392 摘 要 目的:探讨细胞因子对小鼠α2(I)型前胶原基因上游启动子活性的影响。方法:以小鼠α2(I)型前胶原基因启动子(-2 kb~+54 bp)为靶序列,将它与氯霉素乙酰基转移酶(CAT)报告基因组成的重组体pAZ1009用脂质体法转染至胶原产生细胞NIH/3T3细胞,讨论IFNα、IFNγ、TNFα对小鼠α2(I)型前胶原基因上游启动子活性的影响。结果:TNFα抑制小鼠α2(I)型前胶原基因启动子活性,TNFα分别与IFNγ、IFNα联合应用能加强这种抑制作用。结论:TNFα分别与IFNγ、IFNα联合应用能加强抑制作用,这可能与IFNγ、IFNα诱导TNFα受体表达,从而加强TNFα抑制作用有关,而IFNγ抑制胶原蛋白合成作用与该序列无直接相关。 关键词 细胞因子 胶原 基因
The effect of cytokines on promoter activity of α2(I)procollagen gene
GAO Chun-Fang, YIN Tong, WANG Hao et al. Clinical Immunology Center, Changzheng Hospital , Shanghai 200003
Abstract Objective: To study the effect of cytokines on promoter activity of α2(I) procollagen gene. Methods: This study focused on the promoter sequence -2 kb ~ +54 bp of mouse α2(I) procollagen gene and the effect of TNFα, IFNα, IFNγ on promoter activity. The construction pAZ1009 containing this sequence and CAT as reporter gene was transfected to cytokines-treated NIH/3T3 cells with liposomal transfection method. Cytokines treatment was continued for another 24 hours after transfection. Results: The study reveals that TNFα inhibits promoter activity of mouse α2(I) procollagen gene, this inhibition effect is even stronger when TNFα was used in combination with IFNγ or IFNα. Conclusion: A potential explanation for this synergism is provided by the finding that IFNγ, IFNα can increase the number of TNFα receptor, thus making these cells more susceptible to TNFα modulation. The inhibition effect of IFNγ on procollagen production seems have no direct relation with the promoter sequence. Key words Cytokines Collagein Gene
胶原蛋白异常沉积是危及机体多种器官的纤维化疾病的重要特征,肺、肝脏、肾脏、心脏、皮肤等均可能是这种纤维化损伤的靶器官。研究表明,过度沉积的胶原蛋白如I型胶原与其产生细胞相应基因的激[1] [2] 下一页 上一个医学论文: 柯萨基B3病毒感染增强单个核细胞与心脏微血管内皮细胞的粘附 下一个医学论文: 树突状细胞对小鼠实验性自身免疫性甲状腺炎的作用
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