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Differentially regulated expression of the G-protein-coupled receptor
kinases, betaARK and GRK6, during myelomonocytic cell development in vitro
RP Loudon, B Perussia and JL Benovic
Department of Pharmacology, Kimmel Cancer Institute, Thomas Jefferson
University, Philadelphia, PA 19107, USA.
G-protein-coupled receptor kinases (GRKs) mediate agonist-specific
phosphorylation and desensitization of G-protein-coupled receptors.
Previous studies have shown that several of these kinases are expressed in
hematopoietic cells and that GRK expression is modulated during T-
lymphocyte activation. Here, we analyzed the regulation of beta- adrenergic
receptor kinase (betaARK) and GRK6 expression and activity in
myelomonocytic and lymphoid cells. In the promyelocytic cell line HL- 60,
GRK6 protein levels and activity rose twofold to fourfold over the course
of treatment with agents that induce differentiation toward either the
myeloid (dimethyl sulfoxide and retinoic acid) or monocytic
[1alpha,25(OH)2-vitamin D3] lineage, whereas betaARK protein levels and
activity were only slightly altered. In contrast, treatment with phorbol
12,13-myristic acetate (PMA) led to a reduction in steady-state levels and
activity of both betaARK and GRK6. Treatment of human lymphocytes with
several polyclonal activators (phytohemagglutinin, anti-CD3 antibody and
interleukin-2) resulted in enhanced betaARK and GRK6 mRNA and protein
levels and increased activity of both kinases. In contrast, PMA and calcium
ionophore treatment significantly elevated GRK6 protein levels, while
decreasing betaARK expression. These data demonstrate that betaARK and GRK6
expression are differentially regulated during myelomonocytic cell
development and lymphocyte activation.
Volume 88,
Issue 12,
pp. 4547-4557,
12/15/1996
Copyright © 1996 by The American Society of Hematology
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