一个功能未知的miRNA: miR-5590-3p在精子发生障碍中的作用机制研究

miR-5590-3p是我们通过高通量miRNA测序技术筛选获得的人鼠高度同源、差异高表达于严重少弱精子症的miRNA。前期发现，miR-5590-3p过表达诱导生精细胞凋亡；信息学预测及预实验结果提示KITLG是其下游靶基因；miR-5590-3p过表达抑制KITLG的表达。而文献及预实验结果表明KITLG抑制生精细胞凋亡，以上结果和分析提示miR-5590-3p通过抑制KITLG的表达，诱导生精细胞的凋亡。本研究拟采用过表达/沉默及挽救策略，揭示miR-5590-3p通过KITLG调控生精细胞凋亡的分子机制，并阐明miR-5590-3p在精子发生中的表达规律。有关miR-5590-3p影响生精细胞凋亡的作用及机制均未见报道，本研究将有助于理解精子生成障碍的发病机制，并可能为精子发生障碍的临床治疗提供新的思路和潜在的干预靶标。

miR-5590-3p, a kind of miRNA which is screened from miRNA high-throughput sequencing, is significantly increased in severe oligo-asthenospermic patients and is highly conserved between human and mouse. It is still lack of clear functional coverage in spermatogenesis; bioinformatics analysis and luciferase reporter gene analysis show that KITLG is a candidate target of miR-5590-3p. KITLG plays an important role in spermatogenesis，we proposes that miR-5590-3p plays a significant role on spermatogenesis via the regulation of KITLG. To demonstrate this hypothesis, our study apply overexpression, silent strategy test to verify that the function of miR-5590-3p on spermatogenic failure. The research has a source of innovative, and will help to clarify the mechanism on spermatogenic failure. And may provide a new thinking for clinical treatment and potential target to improve spermatogenesis inspermatogenic failure.