TGF-βl Suppresses Inflammation in Cell Therapy for Intervertebral Disc Degeneration

被引:74
|
作者
Yang, Huilin [1 ]
Cao, Cheng [1 ]
Wu, Chunshen [1 ]
Yuan, Chenxi [1 ]
Gu, Qiaoli [1 ]
Shi, Qing [1 ]
Zou, Jun [1 ]
机构
[1] Soochow Univ, Affiliated Hosp 1, Dept Orthopaed Surg, Suzhou 215006, Jiangsu, Peoples R China
来源
SCIENTIFIC REPORTS | 2015年 / 5卷
基金
中国国家自然科学基金;
关键词
MESENCHYMAL STEM-CELLS; NF-KAPPA-B; TRANSPLANTATION; EXPRESSION; ALPHA; INDUCTION;
D O I
10.1038/srep13254
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Recent studies suggest that cell therapy may be an effective way to repair intervertebral disc degeneration. As a strong immune suppressor, TGF-beta 1 has been shown to inhibit inflammation respond effectively. The objective of this study was to explore the effects of TGF-beta 1 during bone marrow mesenchymal stem cells-based therapy for disc degeneration. In vitro assays demonstrated that co-culturing of nucleus pulposus cells with bone marrow mesenchymal stem cells resulted in significantly higher levels of TGF-beta l secretion. This increase inhibited I kappa B phosphorylation and NF-kappa B activation, detected by western blot analysis. Meanwhile, in a rabbit model, MRI analysis revealed significant recovery of signal intensity in the degenerative discs of rabbits receiving cells transplantation, than receiving cells treated with a TGF-beta 1 inhibitor or saline. These findings indicated that enhanced TGF-beta 1 production recovered the degeneration of intervertebral disc. And also immunohistochemical staining detected enhanced collagen II expression in the rabbits treated with cell transplantation. However, the NF-kappa B positive cells were significantly less than other two control groups. Thus, cell therapy promoted TGF-beta 1 expression in nucleus pulposus, leading to anti-inflammatory effects via the inhibition of NF-kappa B, and the amelioration of disc degradation due to increased expression of collagen II and aggrecan in degenerative intervertebral disc.
引用
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页数:10
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