摘要
目的:在细胞水平探索miR-29c在肾脏纤维化中的作用。方法:检测TGF-β1对大鼠肾间质成纤维细胞的促纤维化作用及该过程中miR-29c表达的变化。miRanda和高通量测序找出miR-29c的靶基因。通过转染miR-29c mimics(高表达),检测其对胶原I(Col I)表达的影响。结果:TGF-β1能刺激大鼠肾间质成纤维细胞转分化;大鼠肾间质成纤维细胞转分化后miR-29c表达下调;上调miR-29c能抑制TGF-β1的促转分化作用。结论:miR-29c mimics通过有效抑制TGF-β1刺激NRK-49F细胞株Col I表达起到抗纤维化作用,人工合成的miR-29c mimics转染NRK-49F细胞株有效提高miR-29c表达量从而抑制Col I表达,为治疗肾间质纤维化提供了一个新的靶点。
Objective： To explore the role of miR-29c in rat renal fibrosis. Methods：In order to examine transforming growth factor- β1 （TGF- β1） effect on miR-29c and collagen synthesis, rat renal fibroblast cells were treated with TGF-8 1 for different periods of time and concentration. The target gene of miR-29c was forecasted through MiRanda and high- throughput sequencing. Over-expression and down-regulation of miR-29c by miR-29c mimics and inhibitor. Results： TGF-β1 reduced expression of the miR-29c, which targets collagen I expression,and collagen I proteins are increased. Up-regulation of miR-29c could inhibit the effect of TGF-β1 on transdifferentiation, down-regulation of miR-29c can promote the effect of TGF- β1 on transdifferentiation. Conclusion： miR-29c reversal of the profibrotic effects of TGF-β1 on rat renal interstitial fibroblasts, miR-29c may have potential therapeutic for progressive renal fibrosis.
出处
《温州医学院学报》
CAS
2012年第5期413-418,共6页
Journal of Wenzhou Medical College
基金
国家自然科学基金资助项目(30871179/C140405)
