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作 者:陈伟[1] 梁东[1] 姚翠微[1] 陶静莉[1] 陈孝文[1] 刘华锋[1]
机构地区:[1]广东医学院附属医院肾脏病研究所,广东湛江524001
出 处:《细胞与分子免疫学杂志》2009年第7期609-611,共3页Chinese Journal of Cellular and Molecular Immunology
基 金:广东省自然科学基金资助项目(5011589)
摘 要:目的:探讨白细胞介素-18(IL-18)是否通过核因子-κB(NF-κB)细胞内信号转导途径诱导近端肾小管上皮细胞转分化。方法:实验分单纯IL-18刺激组和SN50预孵育组,单纯IL-18刺激组采用终浓度分别为0、1、10、100μg/L的IL-18处理人肾小管上皮细胞株(HK-2细胞)72h,SN50预孵育组在此基础上预先应用终浓度为100mg/L的NF-κB特异性抑制剂SN50预处理细胞0.5h。然后应用免疫细胞化学法检测HK-2细胞E-cadherin的表达百分数;采用RT-PCR法检测HK-2细胞E-cadherin mRNA的表达。结果:NF-κB特异性抑制剂SN50可拮抗IL-18对HK-2细胞E-cadherin mRNA和蛋白表达的抑制作用。结论:IL-18可通过核因子-κB(NF-κB)细胞内信号转导途径诱导近端肾小管上皮细胞转分化。AIM: To explore the effect of NF-κB signaling pathway in interleukin-18-induced transdifferentiation in renal proximal tubular cells. METHODS: In IL-18 stimulation groups, HK-2 cells were challenged with different concentrations (0, 1, 10, 100μg/L) of IL-18 for 72h; In SN50 preincubation groups, HK-2 cells were incubated with 100 mg/L SN50 for 30 min before IL-18 was added. At the end of the incubation, the expression of E-cadherin was determined by the combination of immunocytochemistry and RT-PCR. RESULTS: Percentage of E-cadherin positive expression HK-2 cells was decreased by IL-18 in dosage dependant manner. Expression of E-cadherin mRNA in HK-2 cells was also decreased by IL-18 in dosage dependant manner. Recovered the mostly part of expression of E-cadherin was found after HK-2 cells were pretreated with SN50. CONCLUSION: IL-18-induced transdifferentiation of RTECs is suppressed by blocking NF-κB signaling pathway. IL-18-induced transdifferentiation of RTECs at least is partly via NF-κB pathway.
关 键 词:上皮细胞-间充质细胞转分化 IL-18 NF-κB 肾小管上皮细胞
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