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TGF-beta inhibits IL-1beta-activated PAR-2 expression through multiple pathways in human primary synovial cells
BMC: Journal of Biomedical Science, 10/26/09
Tsai SH et al. – TGF–could prevent OA from progression with the anabolic ability to induce CTGF production to maintain extracellular matrix (ECM) integrity and to down regulate PAR–2 expression, and the anti–catabolic ability to induce Tissue inhibitors of metalloproteinase–3 (TIMP–3) production to inhibit MMPs leading to avoid PAR–2 over–expression. Because IL–1–induced PAR–2 expressed in hPSCs might play a significantly important role in early phase of OA, PAR–2 repression by exogenous TGF– or other agents might be an ideal therapeutic target to prevent OA from progression.
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Multilocus methylation analysis in a large cohort of 11p15-related foetal growth disorders (Russell Silver and Beckwith Wiedemann syndromes) reveals simultaneous loss of methylation at paternal and maternal imprinted loci
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