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Two signal transduction pathways mediate interleukin-1 receptor expression in Balb/c3T3 fibroblasts
P D Bonin1, W J Chiou, J E McGee
1Department of Cardiovascular Pharmacology, Lilly Research Laboratories, Indianapolis, Indiana 46285.
The Journal of Biological Chemistry
|October 25, 1990
Summary
Platelet-derived growth factor (PDGF) and cAMP pathways independently regulate interleukin-1 receptor (IL-1R) gene expression in fibroblasts. These findings reveal distinct signaling mechanisms controlling IL-1R levels.
Area of Science:
- Cellular and Molecular Biology
- Signal Transduction
- Immunology
Background:
- Previous research established platelet-derived growth factor (PDGF) modulation of interleukin-1 (IL-1) activity and binding.
- PDGF influences IL-1 receptor (IL-1R) gene expression, a key component in IL-1 signaling.
Purpose of the Study:
- To investigate the signal transduction pathways involved in PDGF-mediated IL-1R gene expression.
- To determine if protein kinase C (PKC) and cAMP pathways independently regulate IL-1R expression.
Main Methods:
- Balb/c3T3 fibroblasts were treated with PDGF, phorbol 12-myristate 13-acetate (PMA), staurosporine, and cAMP-stimulating agents.
- IL-1 receptor mRNA levels and 125I-IL-1 binding were quantified.
- PKC activity was modulated using PMA and staurosporine.
Main Results:
- PDGF treatment increased IL-1R mRNA and 125I-IL-1 binding by 10-20 fold.
- Activation of PKC (via PMA) and cAMP pathways both stimulated IL-1R expression.
- PKC inhibition blocked PDGF/PMA-induced IL-1R expression, while cAMP pathway stimulation was independent of PKC.
Conclusions:
- Two distinct signal transduction pathways, one involving PKC and the other cAMP, mediate IL-1R expression in Balb/c3T3 cells.
- These pathways appear to operate independently, suggesting complex regulation of IL-1R levels.