Premium
PDGF‐BB induces vascular smooth muscle cell expression of high molecular weight FGF‐2, which accumulates in the nucleus
Author(s) -
Pintucci Giuseppe,
Yu PeyJen,
Saponara Fiorella,
KadianDodov Daniella L.,
Galloway Aubrey C.,
Mignatti Paolo
Publication year - 2005
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20505
Subject(s) - platelet derived growth factor receptor , vascular smooth muscle , microbiology and biotechnology , fibroblast growth factor , growth factor , platelet derived growth factor , extracellular , intracellular , mapk/erk pathway , biology , downregulation and upregulation , cell growth , signal transduction , chemistry , endocrinology , biochemistry , smooth muscle , receptor , gene
Basic fibroblast growth factor (FGF‐2) and platelet‐derived growth factor (PDGF) are implicated in vascular remodeling secondary to injury. Both growth factors control vascular endothelial and smooth muscle cell proliferation, migration, and survival through overlapping intracellular signaling pathways. In vascular smooth muscle cells PDGF‐BB induces FGF‐2 expression. However, the effect of PDGF on the different forms of FGF‐2 has not been elucidated. Here, we report that treatment of vascular aortic smooth muscle cells with PDGF‐BB rapidly induces expression of 20.5 and 21 kDa, high molecular weight (HMW) FGF‐2 that accumulates in the nucleus and nucleolus. Conversely, PDGF treatment has little or no effect on 18 kDa, low‐molecular weight FGF‐2 expression. PDGF‐BB‐induced upregulation of HMW FGF‐2 expression is controlled by sustained activation of extracellular signal‐regulated kinase (ERK)‐1/2 and is abolished by actinomycin D. These data describe a novel interaction between PDGF‐BB and FGF‐2, and indicate that the nuclear forms of FGF‐2 may mediate the effect of PDGF activity on vascular smooth muscle cells. © 2005 Wiley‐Liss, Inc.