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Effect on platelet‐derived growth factor‐induced mitogenesis of double‐stranded RNA: Evidence for an autocrine growth inhibition mediated by interferon‐β
Author(s) -
Forsberg Karin,
Paulsson Ylva,
Westermark Bengt
Publication year - 1988
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041360208
Subject(s) - autocrine signalling , platelet derived growth factor receptor , growth factor , rna , interferon , platelet derived growth factor , beta (programming language) , microbiology and biotechnology , messenger rna , biology , inducer , growth inhibition , receptor , cell growth , chemistry , biochemistry , immunology , gene , computer science , programming language
Stimulation of normal human foreskin fibroblasts with platelet‐derived growth factor (PDGF) was inhibited by the addition of the synthetic double‐stranded RNA polyinosinic‐polycytidylic acid (poly‐I:C) as measured by incorporation of 3 H‐thymidine ( 3 H‐TdR). Single‐stranded polycytidylic or polyinosinic acid had no effect. Double‐stranded RNA is an inducer of interferon‐β (IFN‐β) in fibroblasts. On the mRNA level, an expression of IFN‐β 2 but not of IFN‐β 1 was seen after addition of PDGF and/or poly‐I:C. The inhibition of PDGF‐induced mitogenesis was completely blocked by an antiserum to IFN‐β. Poly‐I:C did not interfere with PDGF binding to its receptor, nor did it block protein synthesis, indicating that the inhibition is not due to a nonspecific toxic effect of the double‐stranded RNA but rather is mediated by IFN‐β. The present study implies that the IFN‐β system in fibroblasts is a very potent autocrine inhibitory pathway.