These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Norepinephrine induction of mitogen-activated protein kinase phosphatase-1 expression in rat pinealocytes: distinct roles of alpha- and beta-adrenergic receptors.
    Author: Price DM, Chik CL, Ho AK.
    Journal: Endocrinology; 2004 Dec; 145(12):5723-33. PubMed ID: 15358679.
    Abstract:
    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 alpha- and beta-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 beta-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 alpha-adrenergic receptors caused only small increases in MKP-1 mRNA and protein and appeared to function primarily in prolonging the beta-adrenergic-stimulated responses. In NE-stimulated pinealocytes, blockade of beta-adrenergic receptors caused a rapid reduction in MKP-1 mRNA, but it had a minimal effect on MKP-1 protein. In contrast, blockade of alpha-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 beta-adrenergic receptor --> protein kinase A pathway to induce transcription and translation of MKP-1 expression and the alpha-adrenergic receptor --> protein kinase C pathway to prolong the stimulated responses through increased stability of the MKP-1 protein.
    [Abstract] [Full Text] [Related] [New Search]