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J. Biol. Chem., Vol. 276, Issue 29, 27335-27344, July 20, 2001
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From the Different types of plasma membrane
receptors engage in various forms of cross-talk. We used cultures of
rat renal mesangial cells to study the regulation of EGF receptors
(EGFRs) by various endogenous G protein-coupled receptors (GPCRs).
GPCRs (5-hydroxytryptamine2A, lysophosphatidic acid,
angiotensin AT1, bradykinin B2) were
shown to transactivate EGFRs through a protein kinase
C-dependent pathway. This transactivation resulted in the
initiation of multiple cellular signals (phosphorylation of the EGFRs
and ERK and activation of cAMP-responsive element-binding protein
(CREB), NF-
G Protein-coupled Receptors Desensitize and
Down-regulate Epidermal Growth Factor Receptors in Renal Mesangial
Cells*
,¶
Nephrology Division, Department of
Medicine, Medical University of South Carolina, Charleston, South
Carolina 29425, the ¶ Research and Medical Specialty Services,
Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South
Carolina 29401, and the § Endocrinology Division, Department
of Medicine, Duke University Medical Center and Geriatric Research,
Education, and Clinical Center, Durham Veterans Affairs Medical Center,
Durham, North Carolina 27710
B, and E2F), as well as subsequent rapid
down-regulation of cell-surface EGFRs and internalization and
desensitization of the EGFRs without change in the total cellular
complement of EGFRs. Internalization of the EGFRs and the
down-regulation of cell-surface receptors in mesangial cells were
blocked by pharmacological inhibitors of clathrin-mediated endocytosis
and in HEK293 cells by transfection of cDNA constructs that encode
dominant negative 
-arrestin-1 or dynamin. Whereas all of the effects
of GPCRs on EGFRs were dependent to a great extent on protein kinase C,
those initiated by EGF were not. These studies demonstrate that GPCRs
can induce multiple signals through protein kinase
C-dependent transactivation of EGFRs. Moreover, GPCRs
induce profound desensitization of EGFRs by a process associated with
the loss of cell-surface EGFRs through clathrin-mediated endocytosis.
*
This work was supported by the Department of Veterans
Affairs (merit award to J. R. R.), the National Institutes of Health (Grants DK52448 and DK54720 to J. R. R. and DK55524 to L. M. L.), a
fellowship from the American Heart Association (to J. S. G.), and a
laboratory endowment jointly supported by the Division of Nephrology,
Medical University of South Carolina and Dialysis Clinics, Inc.
(to J. R. R.).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.
To whom correspondence should be addressed: Rm. 829 Clinical Sciences Building, Medical University of South
Carolina, 171 Ashley Ave., Charleston, SC 29425. Tel.: 843-792-4122;
Fax: 843-792-8399; E-mail: raymondj@musc.edu.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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