The VEGF production by dedifferentiated chondrocytes under synovial fluid stimulation from coxarthrosis and femoral neck fracture patients
10.3760/cma.j.issn.0253-2352.2010.12.008
- VernacularTitle:髋关节骨关节炎与股骨颈骨折患者滑液对去分化软骨细胞VEGF表达的影响
- Author:
Tengbo YU
;
Yongshuai CHENG
;
Kang SUN
;
Jinzhao LIU
;
Zhijie WANG
;
Xuexiao MA
;
Aimin WANG
- Publication Type:Journal Article
- Keywords:
Osteoarthritis,hip;
Femoral neck fractures;
Chondrocytes;
Vascular endothelial growth factors
- From:
Chinese Journal of Orthopaedics
2010;30(12):1206-1210
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the vascular endothelial growth factor (VEGF) expression level by chondrocytes isolated from patients with osteoarthritis (OA) in hip or femoral neck fracture (FNF) and explore the effect of synovial fluid from OA or FNF on secretion of VEGF. Methods The cartilage tissues were collected from 12 patients with OA in hip and 8 patients with FNF. Cartilage was stained with HIM and Safranin O/Fast Green (S/F) method. The damage of cartilage was evaluated using Mankin scores.Cathepsin B which was selected for cell dedifferentiation monitoring marker and VEGF level was detected in the supernatant fluid. The synovial fluid from OA, FNF and DMEM were respectively added to the culture medium to explore their effects on regulating VEGF. Results Cartilage the Mankin scores of OA group were higher than that of FNF group. Chondrocytes gradually lost their original spherical appearance, with Cathepsin B upregulated while VEGF downregulated. The OA synovial fluid can stimulate chongdrocytes to secrete more VEGF than the one from patients with FNF. However, chondrocytes gradually produced less VEGF after passaging. Conclusion Mankin scores had good correlation with chondrocytes' VEGF production in the early stage of primary culture. Chondrocytes showed quick dedifferentiation characteristics in vitro. OA synovial fluid showed abig ger capability in stimulating chondrocytes to express more VEGF, which might indicate that OA synovial fluid participated in the pathological process of OA.
