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Blood, 1 June 2002, Vol. 99, No. 11, pp. 4048-4052
IMMUNOBIOLOGY
Extracellular signal-regulated kinase mediates
granulocyte-macrophage colony-stimulating factor messenger RNA
stabilization in tumor necrosis factor- plus
fibronectin-activated peripheral blood eosinophils
Stéphane Esnault and
James S. Malter
From the Department of Pathology and Laboratory
Medicine, University of Wisconsin Medical School, Madison.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is
critical for promoting the long-term survival of lung- or airway-based eosinophils. Previously, we have shown that fibronectin and tumor necrosis factor  induced autocrine production of GM-CSF that markedly enhanced eosinophil survival. Cytokine release was preceded by
and dependent on messenger RNA (mRNA) stabilization. Here, we show that
mitogen-activated protein kinase (MAPK) activation is responsible for
GM-CSF mRNA stabilization in peripheral blood eosinophils (pbeos).
Activation of extracellular signal-regulated kinase (ERK) but not p38
correlated with GM-CSF mRNA stability. Although ERK inhibition
completely prevented GM-CSF mRNA stabilization, p38 inhibition had a
partial effect. To establish which MAPK was crucial, we transduced
pbeos with dominant-active TatMEK1(E) or TatMKK3b(E) proteins that
selectively phosphorylate ERK or p38, respectively. These studies
showed that ERK but not p38 was sufficient for GM-CSF mRNA
stabilization. These data are in contradistinction to the c-Jun
NH2-termainal kinase-mediated regulation of interleukin 2 and 3 mRNAs and suggest unique regulatory features for GM-CSF mRNA in eosinophils.
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