HK2/AA Stimulation

Aristolochic acid nephropathy (AAN) is characterised by rapidly progressive tubulointerstitial nephritis culminating in end stage renal failure and urothelial malignancy. microRNAs (miRs) are small endogenous post-transcriptional regulators of gene expression implicated in numerous physiological and pathological processes. We aimed to characterise the mechanism of AA induced cell cycle arrest and its regulation by miRs. The microarray experiment was performed to identify differentially regulated microRNAs in human proximal tubulal epithelial cells treated with aristolochic acid (AA). Analysis or differential miR expression in human proximal tubular epithelial cell line (HK-2) treated with 5ug/ml aristolochic acid, control (n=3) vs aristolochic acid (n=3)

马兜铃酸肾病（Aristolochic acid nephropathy, AAN）以快速进展性小管间质性肾炎为特征，最终可进展至终末期肾衰竭与尿路上皮恶性肿瘤。微小RNA（microRNAs, miRs）是一类内源性小型基因表达转录后调控因子，参与诸多生理与病理过程。本研究旨在阐明马兜铃酸诱导的细胞周期阻滞机制及其受miRs的调控模式。为鉴定马兜铃酸（AA）处理的人类近端肾小管上皮细胞中差异表达的微小RNA，本研究开展了基因芯片实验：对经5μg/ml马兜铃酸处理的人类近端肾小管上皮细胞系（HK-2）进行差异微小RNA表达分析，其中对照组（n=3）与马兜铃酸处理组（n=3）