Comparatièe study of the deèelopmental patterns of èasopressin, glucagon, angiotensin II, and α1-adrenergic receptors in the lièer of deèeloping and adult hypothyroid rats

Al, Mohamed; Cantau, Bernard; Chicot, Daniele; Clos, J.

doi:10.1016/0303-7207(87)90125-0

Cited by 4 publications

(1 citation statement)

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“…Hypothyroidism also promotes an improvement in ␤AR coupling that cannot be ascribed to changes in adenylyl cyclase or G s protein (7,33,34) and that could be explained by our reported changes in GRK2 expression. Interestingly, signaling through other GPCRs that play an essential role in hepatic metabolism, such as receptors for vasopressin or angiotensin II, is also altered in hypothyroid animals (35). Agonist stimulation of these receptors leads to a second messenger response similar to that of euthyroid controls despite the reduced number of receptors in such a condition, thus suggesting a better coupling of receptors to the transduction machinery, which would be favored by reduced GRK2 levels.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2001

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GRK2 is a member of the G protein-coupled receptor kinase family that phosphorylates the activated form of beta-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 ( approximately 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 beta-adrenergic receptors or other G protein-coupled receptor regulatory proteins, such as G protein-coupled receptor kinase 5 or beta-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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