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(Received for publication, September 12, 1996, and in revised form, May 5, 1997)
From the A broad array of stressors induce ACTH release
from the anterior pituitary, with consequent stimulation of the adrenal
cortex and release of glucocorticoids critical for survival of the
animal. ACTH stimulates adrenocortical gene expression in
vivo and inhibits adrenocortical cell proliferation. Binding of
ACTH to its G-protein-coupled receptor stimulates the production of
cAMP and activation of the protein kinase A pathway. The
stress-activated protein kinases (SAPKs) (or c-Jun N-terminal kinases)
and the extracellular signal-regulated kinases (ERKs) are members of
the mitogen-activated protein kinase family of serine/threonine
kinases, which have recently been implicated in G-protein-coupled
receptor intracellular signaling. The SAPKs are preferentially induced
by osmotic stress and UV light, whereas the ERKs are preferentially
induced by growth factors and proliferative signals in cultured cells.
In these studies, ACTH stimulated SAPK activity 3-4-fold both in the
adrenal cortex in vivo and in the Y1 adrenocortical cell
line. 12-O-Tetradecanoylphorbol-13-acetate but not cAMP
induced SAPK activity in Y1 cells. The isoquinolinesulfonamide inhibitors H-8 and H-89 blocked ACTH induction of SAPK activity at
protein kinase C inhibitory doses but not at protein kinase A
inhibitory doses. The calcium chelating agent EGTA inhibited ACTH-induced SAPK activity and the calcium ionophore A23187 induced SAPK activity 3-fold. In contrast with the induction of SAPK by ACTH,
ERK activity was inhibited in the adrenal cortex in vivo and in Y1 adrenal cells. Together these findings suggest that ACTH
induces SAPK activity through a PKC and
Ca+2-dependent pathway. The induction of SAPK
and inhibition of ERK by ACTH in vivo may preferentially
regulate target genes involved in the adrenocortical stress responses
in the whole animal.
Volume 272, Number 32,
Issue of August 8, 1997
pp. 20063-20069
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
,
,
and
Departments of Medicine and Developmental
and Molecular Biology, The Albert Einstein Cancer Center, Albert
Einstein College of Medicine, Bronx, New York 10461 and
Department of Medicine, Northwestern University Medical School,
Chicago, Illinois 60611
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