Epidermal Growth Factor Regulates Astrocyte Expression of the Interleukin-4 Receptor via a MAPK-Independent Pathway

Human astrocytes express the interleukin (IL)-4 receptor alpha chain (IL-4Rα) in vitro and in vivo but mechanisms governing astrocyte IL-4Rα expression have not been established. We hypothesized that epidermal growth factor (EGF) and IL-4, agents that profoundly affect astrocyte proliferation, might...

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Bibliographic Details
Published in:	Cellular immunology Vol. 208; no. 1; pp. 18 - 24
Main Authors:	Barna, B.P., Mattera, R., Jacobs, B.S., Drazba, J., Estes, M.E., Prayson, R.A., Barnett, G.H.
Format:	Journal Article
Language:	English
Published:	Netherlands Elsevier Inc 25-02-2001
Subjects:	astrocytes Astrocytes - cytology Astrocytes - drug effects Astrocytes - metabolism Blotting, Western Cells, Cultured DNA - biosynthesis EGF Enzyme Activation - drug effects Epidermal Growth Factor - antagonists & inhibitors Epidermal Growth Factor - pharmacology Flavonoids - pharmacology Gene Expression Regulation - drug effects human Humans IL-4 Interleukin-4 - pharmacology Isoenzymes - antagonists & inhibitors Isoenzymes - metabolism MAPK Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - metabolism Phosphorylation - drug effects receptors Receptors, Interleukin-4 - biosynthesis Receptors, Interleukin-4 - genetics Receptors, Interleukin-4 - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Signal Transduction - drug effects Time Factors Tumor Cells, Cultured IL-4 astrocytes receptors MAPK EGF human
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Summary:	Human astrocytes express the interleukin (IL)-4 receptor alpha chain (IL-4Rα) in vitro and in vivo but mechanisms governing astrocyte IL-4Rα expression have not been established. We hypothesized that epidermal growth factor (EGF) and IL-4, agents that profoundly affect astrocyte proliferation, might also alter IL-4Rα expression. Exposure to EGF for 24 h enhanced IL-4Rα mRNA levels; in contrast, IL-4 yielded no increase. Immunoblotting demonstrated that EGF but not IL-4 increased astrocyte IL-4Rα protein after 2–4 days of exposure. Similarly, EGF but not IL-4 strongly activated phosphorylation of p42/p44 extracellular regulated kinase isoforms, a reaction blocked by the mitogen-activated protein kinase (MAPK) inhibitor, PD98059. PD98059 also blocked EGF-stimulated DNA synthesis but not IL-4Rα mRNA levels, while antibody to the EGF receptor (erbB1) blocked both EGF effects. Data suggest that astrocyte IL-4Rα expression is upregulated by EGF but not by IL-4 in an EGF-receptor-dependent manner and that mechanisms are independent of MAPK activation.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0008-8749 1090-2163
DOI:	10.1006/cimm.2001.1768