Abstract
BackgroundOsteoarthritis (OA) is a joint disease characterized by degradation of cartilage. The etiology of OA is still unclear. Vascular endothelial growth factor (VEGF) plays a key role of angiogenesis in the pathogenesis of OA and contributes to the angiogenesis of NT-1/DCC. Whether or not NT-1/DCC and VEGF interact in regulating angiogenesis of OA cartilage is not known.MethodsHistological studies for CD34, VEGF, and safranin-O staining were performed to determine angiogenesis and cartilage tissue injury. ELISA indicated the level of pro-inflammation cytokines. Immunoblotting, immunoprecipitation, and electrophoretic mobility shift assay (EMSA) were performed to assay the expression and function of NT-1/DCC-VEGF signaling pathway.ResultsOur data indicated that VEGF expression was increased in cartilage tissue from OA rats, while the chondrocytes were disorganized, and cartilage degeneration was increasing in OA rats. The inflammation factors in articular cavity fluid were higher in the OA rats than in the sham. The protein expression of NT-1, DCC, and VEGF were increased in osteoarthritic cartilage. DCC was involved in the positive regulation of osteoarthritic angiogenesis by VEGF. Egr-1 expression was higher in OA rats than in sham rats. Egr-1 is a regulator of DCC promoter activity, and the binding is higher in OA rats than in sham rats.ConclusionOur present study provides a mechanism by which Egr-1 induced angiogenesis via NT-1/DCC-VEGF pathway.
Highlights
Osteoarthritis (OA) is a joint disease characterized by degradation of cartilage
Angiogenesis in cartilage of OA rat To check the angiogenesis in OA rat, the microvessel density in epiphysis tissues of the proximal epiphysis of the tibia was quantified via CD34 staining, and found microvessel density significantly increased in OA cartilage tissue (Fig. 1a, b)
The data showed that Vascular endothelial growth factor (VEGF) expression was increased in cartilage tissue from OA rats (Fig. 1c), indicating that proliferation and migration of endothelial cell were promoted in OA
Summary
The etiology of OA is still unclear. Osteoarthritis (OA) is an age-dependent, chronic, incurable, and destructive joint disease characterized by degradation of cartilage, hypertrophy of chondrocyte, and sclerosis of subchondral bone [1] and is a main cause of pain and disability of older individuals [2]. It seems that no pharmacological agents could prevent and treat OA, and alleviating joint pain could be the only medical option for OA, which is often unsuccessful, leading to total joint replacement [3, 4].
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