Dexamethasone inhibits phosphorylation of histone H3 at serine 10
| Autor: | Yasuyuki Hasegawa, Akira Yamasaki, Masanari Watanabe, Yutaka Hitsuda, Eiji Shimizu, Hiroyuki Sano, Katsuyuki Tomita |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Biophysics
Anti-Inflammatory Agents RNA polymerase II Cytoplasmic Granules Biochemistry Dexamethasone Histones Histone H3 Transcription (biology) Cell Line Tumor medicine Serine Humans Phosphorylation Molecular Biology Cell Line Transformed A549 cell Cell Nucleus biology Tumor Necrosis Factor-alpha Cell Biology Molecular biology Cell nucleus Histone medicine.anatomical_structure biology.protein Tumor necrosis factor alpha RNA Polymerase II |
| Zdroj: | Biochemical and biophysical research communications. 336(4) |
| ISSN: | 0006-291X |
| Popis: | Glucocorticoids are the most effective anti-inflammatory drugs used in the treatment of inflammatory diseases. While phosphorylation of histone H3 at serine 10 (p-Ser10) is one of the histone modifications related to transcription of some inflammation-related genes, the effect of glucocorticoids on p-Ser10 is not established. Here, we investigated the ability of dexamethasone (Dex) to inhibit p-Ser10 expression in response to tumor necrosis factor (TNF-alpha) in the human lung adenocarcinoma cell line A549 and the SV-40-transformed human airway epithelial cell line BEAS-2B. By Western blot analysis in BEAS-2B cells, the expression of p-Ser10 was repressed by pretreatment with Dex, an effect not seen in A549 cells. Flow cytometric analysis at a single-cell level in A549 cells indicated that TNF-alpha treatment caused early induction of p-Ser10 at 15 min, which was inhibited significantly by pretreatment with 10(-5) M Dex. By immunostaining, the p-Ser10 signal appeared as granules in TNF-alpha-treated cells at same sites of phosphorylated RNA polymerase II. In contrast, the signal was scattered in the nuclei of Dex-pretreated cells. These findings suggested that Dex limits airway inflammation by inhibiting p-Ser10 expression and redistributing p-Ser10 away from transcription sites. |
| Databáze: | OpenAIRE |
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