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- and ß-Adrenergic Receptors
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
Address all correspondence and requests for reprints to: Dr. A.K. Ho, Department of Physiology, 7–26 Medical Sciences Building, Edmonton, Alberta, Canada T6G 2H7. E-mail: anho{at}ualberta.ca.
In this study, we investigated the mechanisms through which norepinephrine (NE) regulates MAPK phosphatase-1 (MKP-1) expression in rat pinealocytes. Stimulation with NE (a mixed 
- and ß-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 ß-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 ß-adrenergic-stimulated responses. In NE-stimulated pinealocytes, blockade of ß-adrenergic receptors caused a rapid reduction in MKP-1 mRNA, but it 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 postreceptor level, treatment with dibutyryl cAMP 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 ß-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.
This article has been cited by other articles:
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  A. K. Ho, D. M. Price, W. G. Dukewich, N. Steinberg, T. G. Arnason, and C. L. Chik Acetylation of Histone H3 and Adrenergic-Regulated Gene Transcription in Rat Pinealocytes Endocrinology, October 1, 2007; 148(10): 4592 - 4600. [Abstract] [Full Text] [PDF]
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C. L. Chik, M. T. Wloka, D. M. Price, and A. K. Ho The Role of Repressor Proteins in the Adrenergic Induction of Type II Iodothyronine Deiodinase in Rat Pinealocytes Endocrinology, July 1, 2007; 148(7): 3523 - 3531. [Abstract] [Full Text] [PDF]
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C. L. Chik, T. G. Arnason, W. G. Dukewich, D. M. Price, A. Ranger, and A. K. Ho Histone H3 Phosphorylation in the Rat Pineal Gland: Adrenergic Regulation and Diurnal Variation Endocrinology, April 1, 2007; 148(4): 1465 - 1472. [Abstract] [Full Text] [PDF]
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A. K. Ho, D. L. Terriff, D. M. Price, M. T. Wloka, and C. L. Chik The Role of Inducible Repressor Proteins in the Adrenergic Induction of Arylalkylamine-N-Acetyltransferase and Mitogen-Activated Protein Kinase Phosphatase-1 in Rat Pinealocytes Endocrinology, February 1, 2007; 148(2): 743 - 751. [Abstract] [Full Text] [PDF]
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 M. A. Giembycz and R. Newton Beyond the dogma: novel {beta}2-adrenoceptor signalling in the airways. Eur. Respir. J., June 1, 2006; 27(6): 1286 - 1306. [Abstract] [Full Text] [PDF]
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D. L. Terriff, C. L. Chik, D. M. Price, and A. K. Ho Proteasomal Proteolysis in the Adrenergic Induction of Arylalkylamine-N-Acetyltransferase in Rat Pinealocytes Endocrinology, November 1, 2005; 146(11): 4795 - 4803. [Abstract] [Full Text] [PDF]
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