期刊
MOLECULAR MEDICINE REPORTS
卷 26, 期 3, 页码 -出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2022.12793
关键词
IDD; NPSCs; MCP-1; C-C chemokine receptor type 2
The study observed significant upregulation of MCP-1 in NPSCs cultured in vitro, which inhibited migration, proliferation, and chondrogenic differentiation of NPSCs. MCP-1 exerted its effects by enhancing CCR2 expression, and the effects could be reversed by blocking CCR2 with an inhibitor.
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-alpha and IL-1 beta 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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