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Submitted on July 9, 2004
Accepted on August 30, 2004
- and 
-Adrenergic Receptor-Activated Signaling Mechanisms
Departments of Physiology (D.M.P., A.K.H.) and Medicine (C.L.C), Faculty of Medicine, University of Alberta, Edmonton, Alberta, Canada T6G 2H7
* To whom correspondence should be addressed. E-mail: anho{at}ualberta.ca.
In this study, we investigated the mechanisms through which norepinephrine (NE) regulates mitogen-activated protein kinase phosphatase-1 (MKP-1) expression in rat pinealocytes. Stimulation with NE (a mixed 
- and 
-adrenergic agonist) caused a rapid increase in MKP-1 mRNA and protein that peaked around 1 h post-stimulation and the response was sustained for at least 4 h. Selective activation of -adrenergic receptors with isoproterenol for 1 h caused a similar increase in MKP-1 mRNA and protein as observed with NE but at 3 h, the isoproterenol response was much lower relative to NE. In contrast, selective activation of -adrenergic receptors caused only small increases in MKP-1 mRNA and protein, and appeared to function primarily in prolonging the -adrenergic stimulated responses. In NE-stimulated pinealocytes, blockade of -adrenergic receptors caused a rapid reduction in MKP-1 mRNA, but had a minimal effect on MKP-1 protein. In contrast, blockade of -adrenergic receptors specifically reduced NE-induced MKP-1 protein but not mRNA. At the post-receptor level, treatment with dibutyryl cAMP (DBcAMP) caused parallel increases in MKP-1 mRNA and protein. However, treatment with a protein kinase C activator caused a significant increase in MKP-1 protein but had little effect on MKP-1 mRNA. Together, these results suggest that, in rat pinealocytes, NE activates the -adrenergic receptor protein kinase A pathway to induce transcription and translation of MKP-1 expression, and the -adrenergic receptor protein kinase C pathway to prolong the stimulated responses through increased stability of the MKP-1 protein.
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