Key result
C-reactive protein decreased eNOS activity and activated GSK-3β during endothelial cell activation, effects which were partially reversed by GSK-3β inhibitors TDZD-8 and SB415286.
Why the study?
Does GSK-3β inhibition prevent CRP-induced endothelial cell activation?
Does GSK-3β inhibition prevent CRP-induced endothelial cell activation?
GSK-3β is involved in CRP-induced endothelial cell activation, and its pharmacological inhibition can partially restore endothelial function in vitro.
GSK-3β inhibition may partially restore endothelial function in vitro; leaves open clinical relevance in CRP-driven vascular disease.
C-reactive protein (CRP) is a significant contributor to atherosclerosis and a powerful predictor of cardiovascular risk. The role of CRP in endothelial cell (EC) activation has been extensively investigated, but the underlying mechanisms have not been fully elucidated. The effect of glycogen synthase kinase-3β (GSK-3β) on CRP-induced EC activation was evaluated in this study. We observed that CRP decreased endothelial nitric oxide synthase (eNOS) activity during EC activation. CRP also activated GSK-3β by dephosphorylating its Ser9 level and reducing β-catenin protein expression in a time-dependent manner. We also found that the GSK-3β inhibitors TDZD-8 and SB415286 partially restored eNOS activity and suppressed the release of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 from ECs. These data provide new evidence for the involvement of GSK-3β in EC activation.
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Liu et al. (2013) studied Endothelial cell activation. C-reactive protein (CRP) and GSK-3β inhibitors (TDZD-8 and SB415286) was evaluated on Endothelial nitric oxide synthase (eNOS) activity and release of adhesion molecules. C-reactive protein decreased eNOS activity and activated GSK-3β during endothelial cell activation, effects which were partially reversed by GSK-3β inhibitors TDZD-8 and SB415286.
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