面神经损伤后临床修复效果欠佳，主要与施万细胞（SCs）增殖和去分化能力相关。据报道，环状RNA（circRNA）可调控细胞的增殖和分化。我们前期研究表明损伤后早期SCs内circRNA RCIR和Runx2表达上调，影响周围神经再生。但是RCIR调控Runx2的分子机制未明。预测发现miR-205能结合RCIR和Runx2。因此提出科学假说：RCIR能通过竞争性结合内源性miR-205上调Runx2的表达，影响SCs的增殖、分化，进而影响神经再生。本研究拟通过在细胞体系中上调/下调RCIR的表达，检测miR-205、Runx2的变化及对SCs生物学行为的影响；通过改变细胞miR-205的表达，验证RCIR结合miR-205改变Runx2表达的分子机制；通过建立动物模型调控RCIR在损伤神经的表达，了解RCIR对神经再生的影响，为阐明circRNA在神经再生中的作用奠定理论基础。

After facial nerve injury, its recovery is far from satisfactory. The ability of Schwann cells (SCs) to proliferate and dedifferentiate restricts nerve regeneration. It is proved that to circular RNA RCIR and Runx2 increase after nerve injury, which may also affect nerve regeneration. But how RCIR regulates Runx2 remains unknown. Our analysis showed that both RCIR and Runx2 had binding sites with miR-205. We propose a scientific hypothesis: RCIR up-regulates the expression of Runx2 through competitively binding with endogenous miR-205, which affects the proliferation and differentiation of SCs, and finally takes effect on nerve regeneration. In this study, the expression of RCIR in SCs was up-/down-regulated in vitro, and the changes of Runx2 and mir 205 expression was detected and biological function of SCs was verified; the molecular mechanism of how RCIR affects Runx2 by miR-205 was studied by changing expression in miR-205 in cell system; the expression of RCIR in injured nerves was modified in vivo to understand its effect and mechanism on nerve regeneration. This program will provide a theoretical foundation and elucidate how circRNA takes the role in nerve regeneration.