p38 Mitogen-activated protein kinase modulates expression of tumor necrosis factor-related apoptosis-inducing ligand induced by interferon-γ in fetal brain astrocytes
✍ Scribed by J. Lee; J.-S. Shin; J.Y. Park; D. Kwon; S.-J. Choi; S.-J. Kim; I.-H. Choi
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 239 KB
- Volume
- 74
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
This study describes the involvement of the p38 mitogen‐activated protein kinase (MAPK) during interferon‐γ (IFN‐γ) signaling in fetal brain astrocytes. In some pathological conditions of brain, p38 MAPK transduces stress‐related signals, increases expression of proinflammatory cytokines, and induces cellular damage or apoptosis. In astrocytes, the tumor necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) expression level was increased by IFN‐γ. AG490, a JAK inhibitor, blocked TRAIL expression induced by IFN‐γ. SB203580, a specific p38α and p38β2 MAPK inhibitor, decreased the TRAIL expression induced by IFN‐γ. The phosphorylation of the Ser727 site of STAT1, but not the Tyr701 site, was inhibited by SB203580. These results suggest that p38 MAPK modulates STAT1 phosphorylation in IFN‐γ signaling in fetal brain astrocytes. © 2003 Wiley‐Liss, Inc.