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J. Biol. Chem., Vol. 276, Issue 10, 7187-7194, March 9, 2001
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From the Departments of Endogenous insulin-like growth factor-1
(IGF-I) stimulates growth of cultured human intestinal smooth muscle by
activating distinct mitogen-activated protein (MAP)
kinase-dependent and phosphatidylinositol
3-kinase-dependent signaling pathways. In Rat1 and Balb/c3T3
fibroblasts and in neurons the IGF-I receptor is coupled to an
inhibitory G protein, Gi, which mediates
G
Coupling of the Insulin-like Growth Factor-I Receptor
Tyrosine Kinase to Gi2 in Human Intestinal Smooth
Muscle
G
-DEPENDENT MITOGEN-ACTIVATED PROTEIN KINASE
ACTIVATION AND GROWTH*
§¶ and Medicine and
§ Physiology, Medical College of Virginia of Virginia
Commonwealth University, Richmond, Virginia 23298
-dependent MAP kinase
activation. The present study determined whether in normal human
intestinal smooth muscle cells the IGF-I receptor activates a
heterotrimeric G protein and the role of G protein activation in
mediating IGF-I-induced growth. IGF-I elicited IGF-I receptor tyrosine
phosphorylation, resulting in the specific activation of
Gi2. G subunits selectively
mediated IGF-I-dependent MAP kinase activation;
G
i2 subunits selectively mediated
IGF-I-dependent inhibition of adenylyl cyclase actvity.
IGF-I-stimulated MAP kinase activation and growth were inhibited by
pertussis toxin, an inhibitor of Gi/Go
activation. Cyclic AMP inhibits growth of human intestinal muscle
cells. IGF-I inhibited both basal and forskolin-stimulated cAMP levels.
This inhibition was attenuated in the presence of pertussis toxin. IGF-I stimulated phosphatidylinositol 3-kinase activation, in contrast to MAP kinase activation, occurred independently of
Gi2 activation. These data suggest that IGF-I specifically
activates Gi2, resulting in concurrent
G-dependent stimulation of
MAP kinase activity and growth, and
Gi2-dependent inhibition of cAMP
levels resulting in disinhibition of cAMP-mediated growth suppression.
*
This work was supported by Grant DK49691 from the NIDDK,
National Institutes of Health.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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