miR-10b通过调节CD44影响肾小管细胞粘附能力在泌尿系结石中的应用

尿石症是泌尿外科常见病之一，目前发病率高达10%，严重影响人民的健康及社会生产力。在结石形成过程中，透明质酸、CD44等粘附分子介导了肾小管上皮细胞对晶体的粘附，导致晶体的滞留和生长，是结石形成关键步骤，但具体机制尚不清楚。MicroRNA（miRNA）是一类非编码RNA，在肿瘤领域miRNA被广泛研究，但是在泌尿系结石领域尚未有报道。在前期研究中，我们发现一水草酸钙晶体刺激肾小管上皮细胞后miR-10b的表达下降，通过上调miR-10b的表达，肾小管上皮细胞晶体粘附能力下降。并且通过预测软件发现miR-10b可能具有靶向抑制CD44的功能。因此，我们推测：在肾小管上皮细胞中miR-10b可能通过靶向作用于CD44发挥抑制细胞晶体粘附功能。本项目拟通过研究miR-10b与CD44在尿石形成过程中的作用及分子机制，为进一步阐明尿石症的发病机制和探索尿石形成的初始环节的干预措施提供依据。

Urinary stone is very common in urology, the morbidity is up to 10%. This disease impact the health care of people and cause a lot of damage on social force. Adhesion molecules like hyaluronan and CD44 have great influence in the formation of urinary stone , however, the definit mechnism is still unknown. MiRNA is small noncode RNA, which studied profound in the field of tumor. There is no report of miRNA in the field of renal stone. In our previous study, we found miR-10 in down-regulated in renal cell through the treatment of oxalate crystal. The adhesion of renal cell was decreased by upregulated miR-10b. We also found miR10b may target CD44 through software. Our project want to study the interaction and molecular mechanism between miR-10b and CD44 in pathogenesis of stone. Our purpuse is to study the mechanism of the formation of renal stone.