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作 者:周振海[1] 李小银[1] 李娟[1] 李幼姬[1] 罗绍凯[1] 洪文德[1]
机构地区:[1]中山大学附属第一医院血液内科,广州510080
出 处:《中国免疫学杂志》2007年第9期857-859,863,共4页Chinese Journal of Immunology
摘 要:目的:体外研究多发性骨髓瘤(MM)患者尿本周氏蛋白(BJP)对肾小管上皮细胞(TEC)的转分化作用以探讨MM肾损害的部分机理。方法:将自MM患者尿中提取的κ和λ型BJP各5例以不同浓度与大鼠NRK52E株TEC共同培养72小时,通过倒置显微镜、透射电镜观察TEC形态学改变;采用细胞免疫组织化学法研究细胞骨架标志:细胞角蛋白-18、波形蛋白、α平滑肌肌动蛋白(α-SMA)表达的改变。结果:培养72小时后,光镜下部分细胞拉长呈梭形;透射电镜下细胞变得肥大,细胞中出现与细胞长轴平行的微丝束和致密体;随BJP的浓度增加,NRK52E细胞角蛋白-18表达率逐渐减少,波形蛋白和α-SMA表达率逐渐增加。结论:BJPκ与BJPλ均有促进NRK52E转分化的作用,且随着BJP浓度增加而增强。Objective:To study the effect of BJP from multiple myeloma (MM) patients on the transdifferentiation (TEMT) of rat renal tubular epithelial-myofibroblasts in vitro. Methods:Rat renal tubular epithelial ceil(TEC) NRK52E was subcultured on a 6- well plate(3 x 10S/ml/well) and exposed to BJPK or BJPλ. in concentration 1,5,10 mg/ml for 72 h. The morphological changes were observed by light and transmission electron microscopy, and cell immunohistiochemistry was used to detect the expression of cytokeratin- 18, vimentin and α-SMA. Results:Mter co-cultured with BJPK or BJPλ., NRK52E cells developed elongated shape, and appeared bun- dles of actin microfilaments. The expression of cytokeratin-18 significantly decreased and vimentin, α-SMA significantly increased. Conclusion:Both BJPK and BJPλ. can induce NRK52E TEMT,which may be importmant mechanisms for BJP direct toxicity on TEC.
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