on September 19, 2002
Published online before print September 19, 2002, doi: 10.1161/01.ATV.0000037679.60584.3F
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Submitted on August 22, 2002
Accepted on September 3, 2002
Growth Factors Enhance Interleukin-1ß-Induced Persistent Activation of Nuclear Factor-
B in Rat Vascular Smooth Muscle Cells
Bingbing Jiang *;
From the Vascular Biology Unit, Whitaker Cardiovascular Institute, Department of Medicine, Boston University School of Medicine, Boston, Mass.
* To whom correspondence should be addressed. 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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