Tnfa , Il6 , Cxcl1 , and Adam8 Genes Are the Early Markers After Mouse Tail Intervertebral Disc Injury
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Updated: Jul 29, 2025
A Mouse Model of Lumbar Spine Instability
Published on: April 23, 2021
Jiawei Lu1, Zuozhen Tian, Frances S Shofer
1From the Departments of Orthopedic Surgery (JL, LY, LQ), Physical Medicine and Rehabilitation (ZT, AZS, YZ), Emergency Medicine (FSS), and Pathology and Laboratory Medicine (HS), Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; Department of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China (JL); and Section of Rehabilitation Medicine, Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, Pennsylvania (YZ).
Objectives:
The early molecular events after intervertebral disc injury remain unclear. In this study, we aimed to compare inflammatory markers from 1 day to 4 wks after injury to have a comprehensive understanding of the intervertebral disc response to injury.
Design:
Mouse tail intervertebral disc injury was induced by a needle puncture. Inflammatory marker gene expression and morphological changes were recorded at 1 day, 1 wk, and 4 wks after injury.
Results:
Tnfa , Il6 , and Cxcl1 gene expression peaked at day 1 post-needle puncture of the mouse intervertebral disc, Adam8 gene expression peaked at 1-wk time point, while Tipe2 gene expression was upregulated at week 4 postinjury. F4/80 positive cells, likely to be macrophages, are present as early as day 1 in the injured intervertebral discs and consistently present at week 4 postinjury. Loss of Safranin O staining and increased histological scores of the injured intervertebral discs are consistent with progressive degeneration after injury.
Conclusions:
Inflammatory cytokines including Tnfa precede Tipe2 , suggesting that Tipe2 is likely induced by Tnfa . Upregulation of Adam8 and Cxcl1 gene expression persisted at week 4, suggesting that they play a role in the transition to chronic phase of intervertebral disc degeneration.
