Interleukin-10-Induced CCR5 Expression in Macrophage Like HL-60 Cells: Involvement of Erk1/2 and STAT-3
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- Makuta Yoko
- Department of Biochemistry, Kyoritsu College of Pharmacy
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- Sonoda Yoshiko
- Department of Biochemistry, Kyoritsu College of Pharmacy
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- Yamamoto Daisuke
- Department of Biochemistry, Kyoritsu College of Pharmacy
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- Funakoshi-Tago Megumi
- Department of Biochemistry, Kyoritsu College of Pharmacy
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- Aizu-Yokota Eriko
- Department of Biochemistry, Kyoritsu College of Pharmacy
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- Takebe Yutaka
- National Institute of AIDS Research, Japan
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- Kasahara Tadashi
- Department of Biochemistry, Kyoritsu College of Pharmacy
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説明
As an immunosuppressive and anti-inflammatory cytokine, IL-10 was recently reported to play roles in CCR5 expression in human monocytes. CCR5 promoter regions contain Oct-2, TCF-1α, GATA, and STAT binding sites. Here, we studied the signals involved in the CCR5 expression in IL-10-stimulated cells using the HL-60 cell line. HL-60 cells were stimulated with PMA and differentiated to macrophage-like cells, then stimulated with IL-10. IL-10 induced significant expression of CCR5 protein and CCR5 mRNA in these cells. The induction of CCR5 by IL-10 was inhibited by a MEK-1 inhibitor, PD98059. In addition, IL-10 induced tyrosine (Tyr) phosphorylation of Erk, as well as serine (Ser) and Tyr phosphorylation of STAT-3. Tyr phosphorylation of Erk and Ser phosphorylation of STAT-3 were inhibited by PD98059, while Tyr phosphorylation of STAT-3 was not inhibited by PD98059. DNA binding activity of STAT-3 was observed by the stimulation with IL-10, which was inhibited by PD98059. These results first indicate that Erk1/2 and STAT-3 regulate CCR5 expression, and that Erk-mediated phosphorylation of Ser is required for full stimulation of STAT-3 in CCR5 expression.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 26 (8), 1076-1081, 2003
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204624429184
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- NII論文ID
- 110003655053
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BD3sznslWitQ%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 6619971
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- PubMed
- 12913253
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可