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The expression of PDGF‐α but not PDGF‐β receptors is suppressed in Swiss/3T3 fibroblasts over‐expressing protein kinase C‐α
Author(s) -
Fitzer-Attas Cheryl,
Eldar Hagit,
Eisenbach Lea,
Livneh Etta
Publication year - 1994
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(94)80493-1
Subject(s) - platelet derived growth factor receptor , protein kinase c , autophosphorylation , receptor , microbiology and biotechnology , platelet derived growth factor , growth factor , biology , 3t3 cells , growth factor receptor , epidermal growth factor , tyrosine kinase , signal transduction , cell culture , protein kinase a , kinase , biochemistry , transfection , genetics
The generation and characterization of Swiss/3T3 cells which stably over‐express protein kinase C (PKC)‐α were previously described by us. In these cells over‐expression of PKC‐α reduced the expression of epidermal growth factor (EGF) receptor molecules [(1990) J. Biol. Chem. 265, 13290‐13296]. Here we show that the expression of PDGF‐α receptors, but not PDGF‐β receptors, was specifically decreased in these cells. Not only were the levels of PDGF‐α receptor mRNA transcript and protein significantly diminished in the PKC‐α over‐producing cells, but their ability to respond to short‐ and long‐term growth factor signals was appropriately compromised. This was reflected in a reduced tyrosine autophosphorylation signal in response to PDGF‐AA, as well as in decreased growth rates of PKC‐α over‐expressing cells when supplied with external PDGF‐AA. A similar decrease in PDGF‐α receptors was also demonstrated in parental Swiss/3T3 cells treated with phorbol esters. Our studies imply that PKC‐α is involved in a cellular mechanism suppressing the expression of PDGF‐α receptors in Swiss/3T3 cells. Hence, activation of PKC‐α or alterations in its cellular levels may affect, in turn, the expression of a specific set of cell surface receptors and their responses to external growth factors.