Peripheral nerve lesions are common in clinical practice. However, functional recovery in humans is often insufficient. Schwann cells are driven by complicated transcriptional program during Wallisian degeneration. Of interest, cyclinD1 protein is proved to support axon regeneration. Moreover, cylinD1 activation may affect upstream neuron apoptosis. It is known that CCND1 (encoding gene for cyclinD1) is one of the target gene of the WNT pathway. In this study, we first illustrated the gene expression spectrum change of peripheral nerve on crush injury site in early stage of peripheral nerve repair by using NGS RNA-seq technique. To further validate our RNA-seq analysis, we detected cylinD1 (CCND1 gene-coding protein) by immunohistochemical staining. Our results showed that local cyclinD1 protein expression in the injury nerve tissue was significantly higher than normal nerve, with elevated cyclinD1 protein overall expression and nuclear concentration. This finding suggests that cylinD1 protein is likely to interact with nuclear transcription factors such as β-catenin involved in regulating mechanisms of WNT signaling pathway during peripheral nerve injury repair process. Next, we further detected the expression level of β-catenin. The results showed a significant increase of β-catenin expression in the peripheral injured nerve tissue with obvious nuclear concentration. The results further support the notion that CCND1 gene involved in regulatory mechanisms via the WNT signaling pathway in PNI . In summary, in current study, we first report CCND1 gene and associated signaling pathways significantly up-regulated, then involve in regulation mechanisms by WNT signaling pathway in PNI repair process. However, it is urgent to further study specific role of CCND1 gene and associated signaling pathways in the recovery regulation mechanisms.