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Sequential CCL2 Expression Profile After Disc Injury in Mice.

Mitsufumi Nakawaki1, Kentaro Uchida1, Masayuki Miyagi1

  • 1Department of Orthopedic Surgery, Kitasato University School of Medicine, 1-15-1 Minami-ku Kitasato, Sagamihara City, Kanagawa, 252-0374, Japan.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society
|November 14, 2019
PubMed
Summary

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In intervertebral disc (IVD) injury, tumor necrosis factor-α (TNF-α) stimulates CCL2 chemokine production, recruiting macrophages. These macrophages then differentiate, contributing to IVD pathology and pain.

Area of Science:

  • Orthopaedic Research
  • Immunology
  • Cell Biology

Background:

  • Macrophages and their inflammatory cytokines are implicated in intervertebral disc (IVD) injury and pain.
  • The precise mechanisms of macrophage recruitment to injured IVDs remain unclear.

Purpose of the Study:

  • To investigate the expression dynamics of the chemokine CCL2 in a mouse model of IVD injury.
  • To elucidate the regulatory mechanisms of CCL2-mediated macrophage recruitment in IVD injury.

Main Methods:

  • Utilized a mouse IVD injury model to analyze macrophage infiltration and expression of CCL2, Ccl2 mRNA, Ccr2, Tnfa, and macrophage markers (M1, M2a, M2c).
  • Investigated the effect of tumor necrosis factor-α (TNF-α) on Ccl2 expression in IVD cells in vitro.

Main Results:

Keywords:
CCL2TNF-αintervertebral discmacrophage recruitment

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  • Macrophage percentage increased significantly from day 1 to day 28 post-injury.
  • CCL2 expression (mRNA and protein) was elevated at 1 and 3 days post-injury.
  • TNF-α stimulation increased Ccl2 mRNA and protein expression in IVD cells; M1 and M2 macrophage markers were upregulated post-injury.

Conclusions:

  • TNF-α upregulates CCL2 expression in injured IVDs, driving macrophage recruitment.
  • Recruited macrophages differentiate into M1 and M2 subtypes, suggesting a role in IVD pathology.
  • CCL2 signaling is a key mechanism in macrophage recruitment and subsequent IVD pathology.