Chinese Journal of Tissue Engineering Research ›› 2026, Vol. 30 ›› Issue (34): 8899-8905.doi: 10.12307/2026.881

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Functional characterization of Caspr2 in a mouse model of sciatic nerve injury

Liu Chenglong1, Wei Shanwen2, Zhou Liyu2, Li Di3, Zou Mingming4, Ma Yanxia2, 5   

  1. 1Department of Anesthesiology, Pujiang People’s Hospital, Pujiang 611630, Sichuan Province China; 2Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou 215000, Jiangsu Province, China; 3Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou 215000, Jiangsu Province, China; 4Department of Neurosurgery, The First Medical Center of Chinese PLA General Hospital, Beijing 100853, China; 5Institute of Orthopedics, Soochow University, Suzhou 215006, Jiangsu Province, China
  • Received:2025-09-22 Revised:2026-02-27 Online:2026-12-08 Published:2026-04-13
  • Contact: Ma Yanxia, MS, Experimentalist, Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou 215000, Jiangsu Province, China; Institute of Orthopedics, Soochow University, Suzhou 215006, Jiangsu Province, China Co-corresponding author: Zou Mingming, PhD, Attending physician, Department of Neurosurgery, The First Medical Center of Chinese PLA General Hospital, Beijing 100853, China
  • About author:Liu Chenglong, PhD, Chief physician, Department of Anesthesiology, Pujiang People’s Hospital, Pujiang 611630, Sichuan Province China Wei Shanwen, MS, Technician in charge, Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou 215000, Jiangsu Province, China Liu Chenglong and Wei Shanwen contributed equally to this work.
  • Supported by:
    National Natural Science Foundation of China (Youth Program), No. 81801238 (to LD); Jiangsu University Clinical Medicine Science and Technology Development Fund Project, No. JLY20180167 (to LCL) 

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Abstract: BACKGROUND: The intrinsic molecular mechanisms and regulatory networks underlying peripheral nerve injury still require systematic investigation. Contactin-associated protein-like 2 (Caspr2), a cell adhesion molecule specifically expressed on the axonal surface, plays a crucial role in nerve fiber myelination. However, its dynamic regulatory mechanisms in peripheral nerve regeneration remain unclear. 
OBJECTIVE: To focus on characterizing the functional role of Caspr2 in a sciatic nerve injury model and to elucidate its molecular mechanisms in regulating axonal regeneration in dorsal root ganglion neurons, thereby providing new insights for developing precise repair strategies for peripheral nerve injuries.
METHODS: A sciatic nerve crush injury model was established in ICR mice. qRT-PCR and western blot were used to analyze the transcriptional and protein expression profiles of Caspr2 in dorsal root ganglion tissues. Immunofluorescence staining was employed to detect Caspr2 expression in dorsal root ganglion neurons. A primary dorsal root ganglion neuron culture system was used to construct intervention models: Caspr2 siRNA negative control group, Caspr2 siRNA treatment group, Caspr2 overexpression group, and Caspr2 empty vector control group. Tuj1 immunofluorescence staining and AxioVision image analysis were performed to quantitatively assess axonal regeneration dynamics.
RESULTS AND CONCLUSION: (1) Injury response characteristics: On day 3 post-injury, both mRNA and protein levels of Caspr2 in dorsal root ganglion tissues decreased, with further reduction by day 7. Additionally, Caspr2 expression in dorsal root ganglion neurons was significantly reduced by day 7 post-injury. (2) Loss-of-function effect: Caspr2 siRNA treatment significantly promoted neuronal axon growth. (3) Overexpression effect: Caspr2 overexpression markedly inhibited axonal elongation. These findings indicate that Caspr2 acts as a key inhibitory factor in peripheral nerve regeneration, bidirectionally regulating axonal regenerative capacity and participating in nerve repair.

Key words: peripheral nerve injury, dorsal root ganglion, neuron, Caspr2 protein, axonal regeneration

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