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Vol. 300, Issue 1, 83-90, January 2002
1B- and 1D-Adrenergic Receptors
Exhibit Different Requirements for Agonist and Mitogen-Activated
Protein Kinase Activation to Regulate Growth Responses in Rat 1 Fibroblasts
Division of Pharmaceutical Sciences (B.A.W., D.M., G.R.P.), College
of Pharmacy, and Department of Pharmacology (M.T.P.), College of
Medicine, University of Kentucky, Lexington, Kentucky
We compared DNA replication, protein biosynthesis, and
mitogen-activated protein kinase (MAPK) activity in Rat 1 fibroblasts stably expressing either the 
1B-adrenergic receptor (AR)
or 1D-AR subtypes. Activation of both the
1B-AR and 1D-AR inhibited DNA synthesis
(as assessed by [3H]thymidine incorporation). In
contrast, both receptors stimulated protein biosynthesis (as measured
by [35S]methionine incorporation) and activated
extracellular signal-regulated kinase (ERK)1/2. Importantly, these
responses were agonist-dependent for the 1B-AR, but were
agonist-independent for the 1D-AR. Agonist activation of
the 1B-AR resulted in increased p38 kinase activity, but
not c-Jun NH2-terminal kinase (JNK) activity, whereas the 1D-AR activated JNK but not p38 kinase. Unlike ERK1/2,
JNK activity was increased by agonist treatment in the
1D-AR cells. An ERK1/2-pathway inhibitor PD98059 had no
effect on phenylephrine-mediated inhibition of DNA synthesis in
either cell line but blocked protein biosynthesis mediated by both
receptors. The p38 kinase inhibitor SB203580 blocked
1B-AR effects on [3H]thymidine and
[35S]methionine incorporation in
1B-AR-expressing cells, but had no effect on
1D-AR-mediated growth responses, consistent with the
inability of the 1D-AR to activate p38 kinase.
Therefore, 1B- and 1D-ARs mediated
similar growth responses but differ with respect to the MAPK family
member involved and the requirement for agonist.
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