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Effect of Hypothyroidism on G Protein-Coupled Receptor Kinase 2 Expression Levels in Rat Liver, Lung, and Heart¹

Departamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa (P.P., M.B., F.M.), and Instituto de Investigaciones Biomédicas, Alberto Sols, Consejo Superior de Investigaciones Científicas (M.A.-D., A.M.), Universidad Autónoma, 28049 Madrid, Spain

Address all correspondence and requests for reprints to: Federico Mayor, Jr., Centro de Biología Molecular, Universidad Autónoma, 28049 Madrid, Spain. E-mail: fmayor{at}cbm.uam.es

GRK2 is a member of the G protein-coupled receptor kinase family that phosphorylates the activated form of -adrenergic and other G protein-coupled receptors and plays an important role in their desensitization and modulation. Alterations in thyroid hormone levels have been reported to lead to important changes in adrenergic receptor responsiveness and signaling in a variety of tissues. In this context, we have explored the effects of experimental hypothyroidism on GRK2 protein levels in rat heart, lung, and liver using a specific antibody. Hypothyroid animals show significant up-regulation (50% increase compared with controls) in GRK2 levels in heart and lung at 60 days after birth, whereas a 50% reduction is detected in the liver at this stage. These alterations are selective, as -adrenergic receptors or other G protein-coupled receptor regulatory proteins, such as G protein-coupled receptor kinase 5 or -arrestin-1, display a different pattern of expression changes in the hypothyroid animals. The reported changes in GRK2 levels and in the receptor/kinase ratio predict alterations in adrenergic receptor desensitization and signal transduction efficacy consistent with those observed in thyroid disorders, thus suggesting a relevant role for the modulation of GRK2 expression in this physiopathological condition.

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