Glycogen synthase kinase-3[beta] is involved in C-reactive protein-induced endothelial cell activation

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Date: Aug. 2013
From: Biochemistry (Moscow)(Vol. 78, Issue 8)
Publisher: Springer
Document Type: Report
Length: 2,267 words
Lexile Measure: 1260L

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Abstract :

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-3[beta] (GSK-3[beta]) 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-3[beta] by dephosphorylating its Ser9 level and reducing [beta]-catenin protein expression in a time-dependent manner. We also found that the GSK-3[beta] 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-3[beta] in EC activation. Keywords: GSK-3[beta], CRP, endothelial activation, eNOS, atherosclerosis DOI: 10.1134/S0006297913080087

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Gale Document Number: GALE|A343156862