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Int J Clin Exp Patho · Jan 2014
Comparative StudyDownregulated interleukin 37 expression associated with aggravation of intervertebral disc degeneration.
- Zhong-Yuan Wan, Zhen Sun, Fang Song, Yu-Fei Chen, Wei-Lin Zhang, Hai-Qiang Wang, and Zhuo-Jing Luo.
- Department of Orthopaedics, Xijing Hospital, Fourth Military Medical University Xi'an, Shaanxi, P. R. China.
- Int J Clin Exp Patho. 2014 Jan 1; 7 (2): 656-62.
AbstractInterleukin 37 (IL-37) is an anti-inflammatory cytokine which was proven to be associated with several diseases characterized with excessive-inflammation. The pathologic process of Intervertebral disc degeneration (IVDD) is also companied by uncurbed inflammation, many cytokines were reported presenting in the process. However, there is little IL-37 related knowledge in IVDD up to now. The aim of this study was to investigate whether IL-37 expression in degenerative intervertebral disc (IVD) is different from that in non-degenerative disc and to evaluate the relationship between IL-37 expression, overexpression of pro-inflammatory cytokines and development of degeneration. Human nucleus pulposus samples were obtained from patients with disc degenerative disease and vertebra fractures undergoing discectomy and fusion. Subsequently, expression of IL-37 was assessed by real-time quantitative polymerase chain reaction (RT-PCR) and western blotting. Gene expression level was measured for IL-1α, IL-1β, IL-6, IL-16, TNF-α, TGF-β1 and Smad3. Degree of degeneration was evaluated for MRI with modified Pfirrmann grading system. The results showed that IL-37 had a decreased expression in degenerative samples compared to that in normal samples both at mRNA and protein level. Instead, significant elevated gene expression of IL-1β, IL-16, TNF-α, TGF-β1 and Smad3 were detected in degenerative samples. High correlations were observed between IL-37, IL-1β, IL-16, TGF-β1, Smad3 and degeneration degree of IVD. Downregulation of IL-37 expression appeared to result in overexpression of pro-inflammatory cytokines, such as IL-1β and IL-16, in degenerative IVD and may be a contributor involved in the progression of IVDD.
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