Fibroblasts, far frombeing merely bystander cells, are known to play a specific role in inflammation resolution after an acute injury. As the endogenous "braking signal," resolvins possess potent anti-inflammatory and proresolution actions. We demonstrated that the expression of COX-2 protein was significantly peaked initially at 6 hours but then also at 48 hours after LPS stimulation in lung fibroblasts. PGElevels also peaked at 6 hours, and PGDlevels were increased and peaked at 48 hours. However, no significant change in the protein expression of COX-1 was observed after treatment with LPS in lung fibroblasts. Exogenous resolvin D1 inhibited the first peak of COX-2 expression as well as the production of PGEinduced by LPS. In contrast, exogenous resolvin D1 increased the second peak of COX-2 expression as well as the production of PGDinduced by LPS. In addition, resolvin D1 inhibited COX-2 expression at 6 hours, which was partly through PI3K/AKT and ERK2 signalling pathways. © 2013 Derong Wu et al.
CITATION STYLE
Wu, D., Zheng, S., Li, W., Yang, L., Liu, Y., Zheng, X., … Jin, S. (2013). Novel biphasic role of resolvin D1 on expression of cyclooxygenase-2 in LIPOPOLYSACCHARIDE-STIMULATED LUNG FIBROBLASTS IS PARTLY THROUGH PI3K/AKT and ERK2 pathways. Mediators of Inflammation, 2013. https://doi.org/10.1155/2013/964012
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