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MIF inhibition attenuates intervertebral disc degeneration by reducing nucleus pulposus cell apoptosis and
Zhongchen Dong1, Peng Yang2, Zhongwei Ji3
1Orthopaedic Institute, Department of Orthopaedic Surgery, the First Affiliated Hospital, Suzhou Medical College, Soochow University, Suzhou, Jiangsu, China; Wujin Hospital Affiliated Hospital, Jiangsu University, Changzhou, Jiangsu, China.
Abstract:
Nucleus pulposus cells (NPCs) apoptosis and inflammation are the extremely critical factors of intervertebral disc degeneration (IVDD). Nevertheless, the underlying procedure remains mysterious. Macrophage migration inhibitory factor (MIF) is a cytokine that promotes inflammation and has been demonstrated to have a significant impact on apoptosis and inflammation. For this research, we employed a model of NPCs degeneration stimulated by lipopolysaccharides (LPS) and a rat acupuncture IVDD model to examine the role of MIF in vitro and in vivo, respectively. Initially, we verified that there was a significant rise of MIF expression in the NP tissues of individuals with IVDD, as well as in rat models of IVDD. Furthermore, this augmented expression of MIF was similarly evident in degenerated NPCs. Afterwards, it was discovered that ISO-1, a MIF inhibitor, effectively decreased the quantity of cells undergoing apoptosis and inhibited the release of inflammatory molecules (TNF-α, IL-1β, IL-6). Furthermore, it has been shown that the PI3K/Akt pathway plays a vital part in the regulation of NPCs degeneration by MIF. Ultimately, we showcased that the IVDD process was impacted by the MIF inhibitor in the rat model. In summary, our experimental results substantiate the significant involvement of MIF in the degeneration of NPCs, and inhibiting MIF activity can effectively mitigate IVDD.
Insights
Macrophage migration inhibitory factor (MIF) drives intervertebral disc degeneration (IVDD) by promoting nucleus pulposus cell (NPC) apoptosis and inflammation. Inhibiting MIF effectively mitigates IVDD progression.
Area of Science:
- Biomedical Science
- Cell Biology
- Inflammation Research
Background:
- Intervertebral disc degeneration (IVDD) is a critical condition driven by nucleus pulposus cell (NPC) apoptosis and inflammation.
- The precise mechanisms underlying IVDD remain incompletely understood.
- Macrophage migration inhibitory factor (MIF), a pro-inflammatory cytokine, is implicated in apoptosis and inflammation.
Purpose of the Study:
- To investigate the role of MIF in the pathogenesis of IVDD.
- To explore the therapeutic potential of MIF inhibition in IVDD.
Main Methods:
- Utilized lipopolysaccharide (LPS)-induced NPC degeneration model in vitro.
- Employed a rat acupuncture-induced IVDD model in vivo.
- Assessed MIF expression levels in human IVDD tissues and rat models.
- Administered a MIF inhibitor (ISO-1) to evaluate its effects on apoptosis and inflammation.
- Investigated the involvement of the PI3K/Akt pathway.
Main Results:
- Elevated MIF expression was observed in human IVDD tissues, rat IVDD models, and degenerated NPCs.
- MIF inhibition using ISO-1 significantly reduced NPC apoptosis and suppressed inflammatory cytokine release (TNF-α, IL-1β, IL-6).
- The PI3K/Akt pathway was identified as a key regulator in MIF-mediated NPC degeneration.
- Inhibition of MIF demonstrated a mitigating effect on IVDD progression in the rat model.
Conclusions:
- MIF plays a significant role in the degeneration of nucleus pulposus cells and the progression of IVDD.
- Targeting MIF activity presents a promising therapeutic strategy for mitigating intervertebral disc degeneration.
