Divergent cellular responses to sciatic nerve crush versus transection: bilateral MYCN induction and distinct DRG neuronal responses.

Authors

Shilian Zhou, Ziyan Huang, Zhongyuan Lin, Jingwei Chen, Xinyu Zhang, Diya Wang, Haihua Shu, Fang Ye

Published in

Frontiers in cellular neuroscience. Volume 20. Pages 1922426. Epub Sep 28, 2026.

Abstract

Peripheral nerve injuries can produce regenerative or persistent-disconnection outcomes depending on the injury modality, but the underlying cellular responses and their effects on the central nervous system remain incompletely defined.
We compared sciatic nerve crush (SNC; axonotmesis) and sciatic nerve transection (SNT; neurotmesis) in wild-type, AdvCre;Ai14, and MYCN-eGFP reporter mice. Longitudinal assessments included functional recovery, neuronal injury responses marked by ATF3, IB4-positive sensory-neuron responses, dorsal-horn microglial activation, and spinal MYCN-eGFP signal.
SNC was associated with partial, measure-specific functional recovery, a transient and self-limited ATF3 response, and a limited reduction in IB4-positive neuronal profiles. In contrast, SNT produced persistent axotomy-associated neuronal stress, a reduction in IB4-positive neuronal profiles, and more protracted dorsal-horn microglial activation. MYCN-eGFP intensity was significantly increased above sham levels bilaterally in spinal ventral-horn neurons after both SNC and SNT at postoperative day 7 (POD7), with the greatest acute amplitude observed after SNC. From POD7 to POD14, MYCN-eGFP intensity declined by more than 90% after SNC but by approximately 60% after SNT, indicating distinct temporal patterns between the two injury modalities.
SNC and SNT engage overlapping but quantitatively and temporally distinct cellular programs, including modality-specific dorsal root ganglion neuronal responses associated with functional recovery. These findings refine the interpretation of two widely used peripheral nerve injury models and identify bilateral spinal MYCN-eGFP dynamics as a candidate cellular readout for future mechanistic investigation.

PMID:
42865581
Bibliographic data and abstract were imported from PubMed on 13 Oct 2026.

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