Articular cartilage may be due to physical aging, excessive exercise, overweight resulting in excessive wear of articular cartilage, or subjected to external impact and cause cartilage damage. It may also be due to immune abnormalities or congenital diseases. The osteoarthritis (degenerative arthritis) is the world's most common joint disease. The laboratory in the previous National Science Council Research Project has analyzed the gene polymorphism of fibronectin, of which 1: c.4252 +204 T> A statistically significant difference in genotype case and control groups. The results have been submitted and revised, and in the near future will be accepted for publication (Journal BMC Musculoskelet Disord; manuscript ID: 8240665181103232). The effects of fibronectin fragments to the human articular chondrocytes and meniscal fibrocartilage cells were investigated. Fibronectin fragment (30 kDa) can induce cartilage cells to upregulate cyclooxygenase2 (COX2) inflammatory response, Toll-like receptor 2 (TLR2) immune phenomenon, and a significant increase in IL6 and IL8 expression. Following continuous research in our laboratory, we are proposing a new three-year research project, entitled: Anti-aging effect with the associated mechanism by PRP (platelet-rich plasma) in cartilage: A fibronectin fragment model. PRP could activate and then release many types of growth factors (PDGF, TGF, VEGF, EGF…etc) to stimulate growth and differentiation, promote cell proliferation, migration, differentiation, collagen synthesis, and angiogenesis. The preliminary results of this laboratory has showed that the increased IL6, IL8, and TLR2 by 30kDa fibronectin fragment stimulation could be suppressed by PRP (n = 3). The signal mechanism is associated with AKT and MAPK activation. Thus the hypothesis is PRP effect via inhibition against TLR2, reducing fibronectin fragment caused degenerative arthritis. Therefore, the implementation of programs by year is as follows： First year: Case collected again, for articular chondrocytes, meniscal cells, synovial cell culture, and to investigate the PRP effect on anti-inflammatory response. cDNA microarray analysis to find novel genes will be also carried out. Second year: The main study is to explore the detailed mechanisms including phosphorylation or cytokine Array membrane screening to identify the specific signaling pathways and subsequent effects on cell growth and other functions. Third year: To establish ex vivo models simulate actual arthroscopic treatment of physiological and pathological tissue reactions that may arise, and the reaction results compiled the first two years of the cells, and perform the mechanism analysis of organizational pattern.
|Effective start/end date||8/1/15 → 7/31/16|
- platelet-rich plasma
- Cartilage degeneration
- Toll-like receptor
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