Chondrocyte catabolic response to synovial fluid obtained from different OA joints: deciphering the roles of TLR4-mediated response G. Barreto, D. Nordström, K.K. Eklund Osteoarthritis and Cartilage Volume 24, (April 2016) DOI: 10.1016/j.joca.2016.01.607 Copyright © 2016 Terms and Conditions
Figure 1 OA Primary chondrocytes and HEK-hTLR4 cells response to SF obtained from CMC-I and knee OA patients. (A) Several chondrocyte produced catabolic factors are differentially upregulate by OA SF from CMC-I and knee. All molecules were measured in Luminex xMap technology and are expressed in pg/ml (B). OA SF from CMC-I and knee joint fails to activate HEK-hTLR4 reporter cells. Results are represented as mean and SD. All experiments were replicated in three (n>3) independent experiments. Osteoarthritis and Cartilage 2016 24, DOI: (10.1016/j.joca.2016.01.607) Copyright © 2016 Terms and Conditions
Figure 2 OA primary chondrocyte nitric oxide production and MMP-13 levels LPS-induced levels are inhibited by sTLR4/MD2. (A) Nitric Oxide is upregulated by TLR4 ligands, while sTLR4/MD2 prevent LPS-induce upregulate levels. (B) MMP-13 protein levels upregulation by LPS is inhibited by sTLR4/MD2. Results are represented as mean and SD. All experiments were replicated in at least three (n>3) independent experiments. Osteoarthritis and Cartilage 2016 24, DOI: (10.1016/j.joca.2016.01.607) Copyright © 2016 Terms and Conditions