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

Yang H, Cao C, Wu C, Yuan C, Gu Q, Shi Q, Zou J - Sci Rep (2015)

Bottom Line: As a strong immune suppressor, TGF-β1 has been shown to inhibit inflammation respond effectively.In vitro assays demonstrated that co-culturing of nucleus pulposus cells with bone marrow mesenchymal stem cells resulted in significantly higher levels of TGF-βl secretion.However, the NF-κB positive cells were significantly less than other two control groups.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.

ABSTRACT
Recent studies suggest that cell therapy may be an effective way to repair intervertebral disc degeneration. As a strong immune suppressor, TGF-β1 has been shown to inhibit inflammation respond effectively. The objective of this study was to explore the effects of TGF-β1 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-βl secretion. This increase inhibited IκB phosphorylation and NF-κB 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-β1 inhibitor or saline. These findings indicated that enhanced TGF-β1 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-κB positive cells were significantly less than other two control groups. Thus, cell therapy promoted TGF-β1 expression in nucleus pulposus, leading to anti-inflammatory effects via the inhibition of NF-κB, and the amelioration of disc degradation due to increased expression of collagen II and aggrecan in degenerative intervertebral disc.

No MeSH data available.


Related in: MedlinePlus

TGF-βl immunohistochemical staining (×200).The expression of TGF-βl was more apparent in the BMSCs transplantation group (8 weeks). Quantification of immunohistochemical staining showed that the BMSCs transplantation had significantly higher mean optical density than the TGF-β1 specific inhibitor-treated and saline group. And the expression of TGF-βl also increased over time significantly. (*p < 0.05, compared to BMSCs transplantation group; #p < 0.05, compared to mean optical density at 4 weeks).
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f7: TGF-βl immunohistochemical staining (×200).The expression of TGF-βl was more apparent in the BMSCs transplantation group (8 weeks). Quantification of immunohistochemical staining showed that the BMSCs transplantation had significantly higher mean optical density than the TGF-β1 specific inhibitor-treated and saline group. And the expression of TGF-βl also increased over time significantly. (*p < 0.05, compared to BMSCs transplantation group; #p < 0.05, compared to mean optical density at 4 weeks).

Mentions: To understand that suppression effects of TGF-βl in NF-κB-dependent inflammation are responsible for the protection against rabbit disc degeneration, we next used immunohistochemistry to detect the expressions of TGF-βl and NF-κB. Immunohistochemical analyses revealed that the expression of TGF-βl increased over time in the BMSCs transplantation group, and also the expression in these discs was significantly higher compared to those detected in the saline and SB431542 groups. (p < 0.05) (Fig. 7). However, the expression of NF-κB decreased over time in BMSCs transplantation group. And the expression was significantly lower compared to two control groups. (p < 0.05). On the other hand, the expressions of both TGF-βl and NF-κB in SB431542 group was no significant differences when compared with the saline group. (p > 0.05) (Fig. 8).


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

Yang H, Cao C, Wu C, Yuan C, Gu Q, Shi Q, Zou J - Sci Rep (2015)

TGF-βl immunohistochemical staining (×200).The expression of TGF-βl was more apparent in the BMSCs transplantation group (8 weeks). Quantification of immunohistochemical staining showed that the BMSCs transplantation had significantly higher mean optical density than the TGF-β1 specific inhibitor-treated and saline group. And the expression of TGF-βl also increased over time significantly. (*p < 0.05, compared to BMSCs transplantation group; #p < 0.05, compared to mean optical density at 4 weeks).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4542522&req=5

f7: TGF-βl immunohistochemical staining (×200).The expression of TGF-βl was more apparent in the BMSCs transplantation group (8 weeks). Quantification of immunohistochemical staining showed that the BMSCs transplantation had significantly higher mean optical density than the TGF-β1 specific inhibitor-treated and saline group. And the expression of TGF-βl also increased over time significantly. (*p < 0.05, compared to BMSCs transplantation group; #p < 0.05, compared to mean optical density at 4 weeks).
Mentions: To understand that suppression effects of TGF-βl in NF-κB-dependent inflammation are responsible for the protection against rabbit disc degeneration, we next used immunohistochemistry to detect the expressions of TGF-βl and NF-κB. Immunohistochemical analyses revealed that the expression of TGF-βl increased over time in the BMSCs transplantation group, and also the expression in these discs was significantly higher compared to those detected in the saline and SB431542 groups. (p < 0.05) (Fig. 7). However, the expression of NF-κB decreased over time in BMSCs transplantation group. And the expression was significantly lower compared to two control groups. (p < 0.05). On the other hand, the expressions of both TGF-βl and NF-κB in SB431542 group was no significant differences when compared with the saline group. (p > 0.05) (Fig. 8).

Bottom Line: As a strong immune suppressor, TGF-β1 has been shown to inhibit inflammation respond effectively.In vitro assays demonstrated that co-culturing of nucleus pulposus cells with bone marrow mesenchymal stem cells resulted in significantly higher levels of TGF-βl secretion.However, the NF-κB positive cells were significantly less than other two control groups.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, China.

ABSTRACT
Recent studies suggest that cell therapy may be an effective way to repair intervertebral disc degeneration. As a strong immune suppressor, TGF-β1 has been shown to inhibit inflammation respond effectively. The objective of this study was to explore the effects of TGF-β1 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-βl secretion. This increase inhibited IκB phosphorylation and NF-κB 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-β1 inhibitor or saline. These findings indicated that enhanced TGF-β1 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-κB positive cells were significantly less than other two control groups. Thus, cell therapy promoted TGF-β1 expression in nucleus pulposus, leading to anti-inflammatory effects via the inhibition of NF-κB, and the amelioration of disc degradation due to increased expression of collagen II and aggrecan in degenerative intervertebral disc.

No MeSH data available.


Related in: MedlinePlus