Published online before print September 19, 2002, doi: 10.1161/01.ATV.0000037679.60584.3F
© 2002 American Heart Association, Inc.
Vascular Biology |
Growth Factors Enhance Interleukin-1ß-Induced Persistent Activation of Nuclear Factor-
B in Rat Vascular Smooth Muscle Cells
From the Vascular Biology Unit, Whitaker Cardiovascular Institute, Department of Medicine, Boston University School of Medicine, Boston, Mass.
Correspondence to Bingbing Jiang, PhD, Vascular Biology Unit, Whitaker Cardiovascular Institute, Department of Medicine, Boston University School of Medicine, 650 Albany St, X704, Boston, MA 02118. E-mail bjiang{at}bu.edu
Objective— Activation of extracellular signal-regulated kinases (ERKs) is required for interleukin-1ß to persistently activate nuclear factor (NF)-
B and concomitantly express inducible NO synthase (iNOS) in rat vascular smooth muscle cells (VSMCs). The present study examined whether platelet-derived growth factor (PDGF) or epidermal growth factor (EGF) could influence the VSMC response to interleukin-1ß via an ERK-related signaling pathway.
Methods and Results— Treatment of VSMCs with PDGF or EGF alone potently induced ERK phosphorylation and DNA synthesis but did not induce NF-B activation or iNOS expression. However, either PDGF or EGF markedly enhanced interleukin-1ß-induced persistent NF-B activation and iNOS expression but did not affect the early and transient NF-B activation. Growth factor-induced DNA synthesis was attenuated in the presence of interleukin-1ß. Inhibition of ERK phosphorylation with selective inhibitors (PD98059 or U0126) attenuated interleukin-1ß-induced persistent NF-B activation and iNOS expression in either the absence or presence of the growth factors.
Conclusions— These results indicate that interleukin-1ß-induced expression of NF-B-dependent genes, such as iNOS, is potentiated in the presence of growth factors through a mechanism requiring ERK-dependent enhanced NF-B activation, and the results also suggest that NF-B activation is not required for PDGF or EGF to trigger DNA synthesis in VSMCs.
Key Words: extracellular signal-regulated kinase • growth factors • interleukin-1ß • nuclear factor-B • vascular smooth muscle cells
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