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机构地区:[1]台州市肿瘤医院皮肤科,台州317502 [2]台州中西医结合医院皮肤科,台州317500 [3]台州市肿瘤医院药剂科,台州317502
出 处:《中国免疫学杂志》2016年第1期101-103,共3页Chinese Journal of Immunology
摘 要:目的:探讨P53抑制剂和微管抑制剂对银屑病表皮角质形成细胞糖皮质激素受体(GR)核转运的影响。方法:分离和培养银屑病患者和正常人表皮角质形成细胞,分别与P53抑制剂和微管蛋白抑制剂共培养,加或不加血管内皮细胞生长因子(VEGF),间接免疫荧光法检测上述因素对GR核转位的影响。结果:VEGF可诱导正常角质形成细胞发生核转位;P53抑制剂抑制了VEGF诱导的GR核转位。与VEGF共培养的角质形成细胞的核转位评分显著低于单纯角质形成细胞的核转运评分,差异有统计学意义(P<0.05);微管抑制剂可完全将正常表皮角质形成细胞的GR滞留在胞浆中,在加入VEGF后,与单纯微管抑制剂组比较,胞浆中GR并没有明显增多;而微管抑制剂和P53抑制剂共培养,会有少量GR进入角质形成细胞的胞核中。结论:微管介导银屑病角质形成细胞GR的核摄取,P53参与了GR的核输出。Objective: To investigate the effect of P53 inhibitors and microtubule inhibitors on nuclear translocation of glucocorticoid receptor in psoriatic epidermal keratinocytes. Methods: Isolate and culture psoriatic and normal epidermal keratinocytes. The keratinocytes were incubated with P53 inhibitors and mierotubule inhibitors with or without vascular endothelial growth factor(VEGF) , and then detected the distribution of GR by indirect immunofluorescence. Results: VEGF induced nuclear trans- location of GR in normal keratinoeytes, and the P53 inhibitor restrained VEGF induced nuclear export of GR in normal keratinocytes. The nuclear transloeation score of the keratinocytes cultured with VEGF was significantly lower than that of keratinocytes cultured without VEGF( P〈0. 05 ). The microtubule inhibitors could completely detained GR of normal epidermal keratinoeytes in the cytoplasm, and there's no significantly increased of the level of GR in the cytoplasm after putting VEGF into the normal epidermal kera- tinocytes. While the microtubule inhibitors and P53 inhibitors co-cultured, there will be a small amount of GR into the keratinocyte nuclei. Conclusion: Microtubule mediated uptake of GR, P53 participated nuclear export of GR.
关 键 词:银屑病 糖皮质激素受体 P53抑制剂 微管抑制剂
分 类 号:R758.63[医药卫生—皮肤病学与性病学]
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