NDLI: Role of beta-arrestin1/ERK MAP kinase pathway in regulating adenosine A1 receptor desensitization and recovery.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jajoo, Sarvesh Mukherjea, Debashree Kumar, Sunny Sheth, Sandeep Kaur, Tejbeer Rybak, Leonard P. Ramkumar, Vickram
Description	Country affiliation: United States Author Affiliation: Jajoo S ( PO Box 19629, SIU School of Medicine, Springfield, IL 62794, USA. vramkumar@siumed.edu)
Abstract	Exposure of cells to adenosine receptor (AR) agonists leads to receptor uncoupling from G proteins and downregulation of the A(1)AR. The receptor levels on the cell surface generally recover on withdrawal of the agonist, because of either translocation of the sequestered A(1)AR back to plasma membrane or de novo synthesis of A(1)AR. To examine the mechanism(s) underlying A(1)AR downregulation and recovery, we treated ductus deferens tumor (DDT(1) MF-2) cells with the agonist R-phenylisopropyladenosine (R-PIA) and showed a decrease in membrane A(1)AR levels by 24 h, which was associated with an unexpected 11-fold increase in A(1)AR mRNA. Acute exposure of these cells to R-PIA resulted in a rapid translocation of beta-arrestin1 to the plasma membrane. Knockdown of beta-arrestin1 by short interfering RNA (siRNA) blocked R-PIA-mediated downregulation of the A(1)AR, suppressed R-PIA-dependent ERK1/2 and activator protein-1 (AP-1) activity, and reduced the induction of A(1)AR mRNA. Withdrawal of the agonist after a 24-h exposure resulted in rapid recovery of plasma membrane A(1)AR. This was dependent on the de novo protein synthesis and on the activity of ERK1/2 but independent of beta-arrestin1 and nuclear factor-kappaB. Together, these data suggest that exposure to A(1)AR agonist stimulates ERK1/2 activity via beta-arrestin1, which subserves receptor uncoupling and downregulation, in addition to the induction of A(1)AR expression. We propose that such a pathway ensures both the termination of the agonist signal and recovery by priming the cell for rapid de novo synthesis of A(1)AR once the drug is terminated.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00190.2009
Journal	American Journal of Physiology - Cell Physiology
Issue Number	1
Volume Number	298
Language	English
Publisher	American Physiological Society
Publisher Date	2010-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Arrestins Physiology Extracellular Signal-regulated Map Kinases Metabolism Receptor, Adenosine A1 Animals Genetics Blotting, Western Cell Culture Techniques Cell Division Cricetinae Immunohistochemistry Mesocricetus Muscle, Smooth Cytology Phenylisopropyladenosine Pharmacology Rna, Small Interfering Drug Effects Reverse Transcriptase Polymerase Chain Reaction Transfection Vas Deferens
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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Role of β-arrestin1/ERK MAP kinase pathway in regulating adenosine A1 receptor desensitization and recovery

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