miR-383是非编码RNA家族中miRNA的成员之一。前期研究发现，特发性非梗阻性无精症（NOA）患者睾丸组织miR-383的表达较正常生育男性有显著的下调,并证实miR-383通过靶向调控转录因子IRF1的表达，影响精子的发生。然而，不同病理类型NOA患者间，miR-383的表达是否存在差异？与正常生育男性睾丸组织比较，miR-383发生差异表达的NOA患者睾丸组织mRNA的表达是否存在差异，其调控NOA生精过程又有何种差异？因此本课题拟通过基因芯片、生物信息学方法、免疫印迹实验、报告基因实验、实时定量PCR技术、免疫组化及体外细胞内功能实验等，探索NOA不同病理类型与miR-383差异性调控间的联系，从而进一步揭示miR-383在不同病理类型睾丸生精过程中的上下游调控途径，为深入了解miR-383调控睾丸生精过程（如减数分裂、细胞凋亡）的作用及机制提供基础。

Our previous studies have shown that microRNA-383 (miR-383) expression is downregulated in the testes of infertile men with non-obstructive azoospermia (NOA). In addition, we have confirmed that the effects of miR-383 were mediated through targeting interferon regulatory factor-1 (IRF1),which was contributed to spermatogensis. However, the alteration of miR-383 expression among NOA patients with different pathological types remains unknown. Compared with normal controls, whether there are any differences in mRNA expression profile of infertile with downregulated miR-383 is unclear. In the subjects, we intend to understand the relationship between the degree of spermatogenesis damage and molecular mechanism of miR-383, and further revealed the function and regulatory pathways of miR-383 in testes with difference pathological types using microarray, bioinformatics analysis, western bolt,report gene assay, real-time PCR,immunohistochemistry etc.It would contribute to understand the regulatory mechanism and function of the miR-383 in spermatogenesis （e.g.,meiosis, apoptosis）on infertile men with NOA.