Title : Inhibitor of G protein-coupled receptor kinase 2 normalizes vascular endothelial function in type 2 diabetic mice by improving β-arrestin 2 translocation and ameliorating Akt/eNOS signal dysfunction.

Pub. Date : 2012 Jul

PMID : 22581458






3 Functional Relationships(s)
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1 The GRK2 inhibitor significantly improved clonidine-induced relaxation only in diabetic (ob/ob and DM) mice, with accompanying attenuations of GRK2 activity and translocation to the plasma membrane. Clonidine G protein-coupled receptor kinase 2 Mus musculus
2 These protective effects of the GRK2 inhibitor may be attributable to the augmented Akt/eNOS pathway activation (as evidenced by increases in Akt phosphorylation at Ser(473) and at Thr(308), and eNOS phosphorylation at Ser(1177)) and to the prevention of the GRK2 translocation and promotion of beta-arrestin 2 translocation to the membrane under clonidine stimulation. Clonidine G protein-coupled receptor kinase 2 Mus musculus
3 Our work provides the first evidence that in diabetes, the GRK2 inhibitor ameliorates vascular endothelial dysfunction via the Akt/eNOS pathway by inhibiting GRK2 activity and enhancing beta-arrestin 2 translocation under clonidine stimulation, thereby contributing to a blood pressure-lowering effect. Clonidine G protein-coupled receptor kinase 2 Mus musculus