Efficiency of magnetic liposomal transforming growth factor-beta 1 in the repair of articular cartilage defects in a rabbit model

2005 ◽  
Vol 73A (3) ◽  
pp. 255-263 ◽  
Author(s):  
Haruyuki Tanaka ◽  
Takashi Sugita ◽  
Yuji Yasunaga ◽  
Shouji Shimose ◽  
Masataka Deie ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Rabbit Model ◽  
Cartilage Defects ◽  
Growth Factor Beta ◽  
Articular Cartilage Defects

scholarly journals Mechanical stress contributes to osteoarthritis development through the activation of transforming growth factor beta 1 (TGF-β1)

2018 ◽  
Vol 7 (11) ◽  
pp. 587-594 ◽  
Author(s):  
R-K. Zhang ◽  
G-W. Li ◽  
C. Zeng ◽  
C-X. Lin ◽  
L-S. Huang ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Growth Factor ◽  
Cyclic Loading ◽  
Mechanical Stress ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cartilage Degradation ◽  
Growth Factor Beta ◽  
Tgf Β1 ◽  
Cultured Chondrocytes

Objectives The role of mechanical stress and transforming growth factor beta 1 (TGF-β1) is important in the initiation and progression of osteoarthritis (OA). However, the underlying molecular mechanisms are not clearly known. Methods In this study, TGF-β1 from osteoclasts and knee joints were analyzed using a co-cultured cell model and an OA rat model, respectively. Five patients with a femoral neck fracture (four female and one male, mean 73.4 years (68 to 79)) were recruited between January 2015 and December 2015. Results showed that TGF-β1 was significantly upregulated in osteoclasts by cyclic loading in a time- and dose-dependent mode. The osteoclasts were subjected to cyclic loading before being co-cultured with chondrocytes for 24 hours. Results A significant decrease in the survival rate of co-cultured chondrocytes was found. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling (TUNEL) assay demonstrated that mechanical stress-induced apoptosis occurred significantly in co-cultured chondrocytes but administration of the TGF-β1 receptor inhibitor, SB-505124, can significantly reverse these effects. Abdominal administration of SB-505124 can attenuate markedly articular cartilage degradation in OA rats. Conclusion Mechanical stress-induced overexpression of TGF-β1 from osteoclasts is responsible for chondrocyte apoptosis and cartilage degeneration in OA. Administration of a TGF-β1 inhibitor can inhibit articular cartilage degradation. Cite this article: R-K. Zhang, G-W. Li, C. Zeng, C-X. Lin, L-S. Huang, G-X. Huang, C. Zhao, S-Y. Feng, H. Fang. Mechanical stress contributes to osteoarthritis development through the activation of transforming growth factor beta 1 (TGF-β1). Bone Joint Res 2018;7:587–594. DOI: 10.1302/2046-3758.711.BJR-2018-0057.R1.

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