Articular cartilage disease, including cartilage degeneration, rheumatoid disease, gout arthropathy, can cause cartilage irreversible destruction in which degenerative arthritis is the most common joint disease in the world and in Taiwan as well. PRP (platelet-rich plasma) is the plasma containing a high concentration of platelets. The patient's blood after centrifugation and purification, a high concentration of platelets obtained from the serum of the layered, and then released by the activation of a multi-class growth factor, the cells will be able to play the efficient stimulation of the growth and differentiation capacity. Such as platelet-derivative growth factor (PDGF), transforming growth factor (TGF), vascular endothelial cell growth factor (VEGF), epidermal growth factor (EGF), insulin-like growth factor (IGF), fibroblast growth factor (FGF), connective tissue growth factor (CTGF), and keratinocyte growth factor (KGF), can promote cell proliferation, migration, differentiation, collagen synthesis, and angiogenesis. Fibronectin is a kind of non-collagenous glycoprotein with important biological activity, is an important component of the extracellular matrix, and involves in the adhesion of the cell proliferation and differentiation, signal transduction, gene expression, tissue repair, immune regulation and other important physiological functions. Higher protease degradation fragment was found in the cartilage and synovial fluid in patients with arthritis. Once fibronectin into small fragments of debris will have catalytic activity, also induce cartilage destruction, and cause the degenerative arthritis. The laboratory research project last year supported by the National Science Council identified the fibronectin gene polymorphism in 1: c.4252 +204 T>A between the case group and the control group with statistical significant difference, but the integrin had no significant association. Also found that fibronectin fragments can produce the inflammatory reaction with cyclooxygenase 2 increase in articular chondrocytes, and induce the increased expression of Toll-like receptor 2 (TLR2). Therefore a new three-year research project is conducted and entitled “Platelet-rich plasma effects in the articular chondrocytes and synovial fibroblasts with the associated mechanism: A fibronectin fragment model” to explore the effectiveness of its treatment. The laboratory already had preliminary results (n = 3), primary cultured cartilage cells by the 30kD fragment increased TLR2 significantly. Different fragments on the reaction of different TLR types have yet to draw firm conclusions. PRP on TLR2 rise significantly inhibited under the mechanism of AKT and MAPK activation. Therefore, the executive of the plan and years as follows: First year: Collect more cases for primary cultures to explore the PRP effects on the anti-inflammatory and TLR2 expression. cDNA microarray analysis will be carried out to look for genes that influence. Second year: The more detailed mechanisms by more cases including signal transduction and phosphorylation will be carried out to identify the specificity of signaling pathways and subsequent impact on cell growth and other functions. Third year: Establish the ex vivo model to simulate the actual arthroscopic treatment under physiological and pathological reactions and collecting data from previous cell research to examine the tissue model.
|Effective start/end date||8/1/13 → 7/31/14|
- Cartilage degeneration
- platelet-rich plasma
- Toll-like receptor
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