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Article

MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells

  • Authors:
    • Xuancheng Ou
    • Tianyong Wen
    • Jinwei Ying
    • Qing He
    • Anwu Xuan
    • Dike Ruan
  • View Affiliations / Copyright

    Affiliations: Department of Spine Surgery, The Central Hospital of Yongzhou, Yongzhou, Hunan 425000, P.R. China, Department of Orthopedic Surgery, The Sixth Medical Centre of PLA General Hospital, Beijing 100053, P.R. China, Department of Orthopedic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
  • Article Number: 277
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    Published online on: July 15, 2022
       https://doi.org/10.3892/mmr.2022.12793
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Abstract

Intervertebral disc degeneration (IDD) creates a hostile environment with high osmotic pressure, high mechanical stress, hypoxia and a low pH, where cytokines such as TNF‑α and IL‑1β are highly expressed. The degenerating intervertebral disc has high local expression of monocyte chemoattractant protein‑1 (MCP‑1), which is associated with the degree of degeneration. However, there are a few reports on the influence of MCP‑1 on nucleus pulposus‑derived stem cells (NPSCs). In the present study, a significant upregulation of MCP‑1 was observed in NPSCs cultured in vitro with pro‑inflammatory cytokines. MCP‑1 significantly inhibited the migration and proliferation of NPSCs in a dose‑dependent manner as detected via Cell Counting Kit‑8, wound healing and Transwell assays. Western blotting and histological analysis demonstrated that MCP‑1 significantly reduced chondrogenic NPSC differentiation. Reverse transcription‑quantitative PCR and western blotting revealed that C‑C chemokine receptor type 2 (CCR2) mRNA and protein expression levels were significantly enhanced by MCP‑1. Furthermore, MCP‑1 significantly inhibited the migration, differentiation and proliferation of NPSCs, which was effectively reversed by blocking CCR2 with the inhibitor RS504393. Overall, these results demonstrated that MCP‑1 may contribute to the inhibition of chondrogenic NPSC differentiation via MCP‑1/CCR2 chemotaxis signals, providing a potential therapeutic target for IDD.
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Copy and paste a formatted citation
Spandidos Publications style
Ou X, Wen T, Ying J, He Q, Xuan A and Ruan D: MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells. Mol Med Rep 26: 277, 2022.
APA
Ou, X., Wen, T., Ying, J., He, Q., Xuan, A., & Ruan, D. (2022). MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells. Molecular Medicine Reports, 26, 277. https://doi.org/10.3892/mmr.2022.12793
MLA
Ou, X., Wen, T., Ying, J., He, Q., Xuan, A., Ruan, D."MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells". Molecular Medicine Reports 26.3 (2022): 277.
Chicago
Ou, X., Wen, T., Ying, J., He, Q., Xuan, A., Ruan, D."MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells". Molecular Medicine Reports 26, no. 3 (2022): 277. https://doi.org/10.3892/mmr.2022.12793
Copy and paste a formatted citation
x
Spandidos Publications style
Ou X, Wen T, Ying J, He Q, Xuan A and Ruan D: MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells. Mol Med Rep 26: 277, 2022.
APA
Ou, X., Wen, T., Ying, J., He, Q., Xuan, A., & Ruan, D. (2022). MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells. Molecular Medicine Reports, 26, 277. https://doi.org/10.3892/mmr.2022.12793
MLA
Ou, X., Wen, T., Ying, J., He, Q., Xuan, A., Ruan, D."MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells". Molecular Medicine Reports 26.3 (2022): 277.
Chicago
Ou, X., Wen, T., Ying, J., He, Q., Xuan, A., Ruan, D."MCP‑1/CCR2 axis inhibits the chondrogenic differentiation of human nucleus pulposus mesenchymal stem cells". Molecular Medicine Reports 26, no. 3 (2022): 277. https://doi.org/10.3892/mmr.2022.12793
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