Involvement of proton-sensing receptor TDAG8 in the anti-inflammatory actions of dexamethasone in peritoneal macrophages

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• 作者：Xiao-dong  ; He ; Masayuki  ; Tobo ; Chihiro  ; Mogi ; Takashi  ; Nakakura ; Mayumi  ; Komachi ; Naoya  ; Murata ; Mutsumi  ; Takano ; Hideaki  ; Tomura ; Koichi  ; Sato ; Fumikazu  ; Okajima  ; ;   ; ^{fokajima@showa.gunma-u.ac.jp}
• 关键词：Glucocorticoid ; TDAG8 ; Acidification ; TNF-¦Á ; Cell death ; Macrophage
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2011
• 出版时间：2 December 2011
• 年：2011
• 卷：415
• 期：4
• 页码：627-631
• 全文大小：231 K

文摘

Dexamethasone (DEX), a potent glucocorticoid, increased the expression of T-cell death associated gene 8 (TDAG8), a proton-sensing G protein-coupled receptor, which is associated with the enhancement of acidic pH-induced cAMP accumulation, in peritoneal macrophages. We explored the role of increased TDAG8 expression in the anti-inflammatory actions of DEX. The treatment of macrophages with either DEX or acidic pH induced the cell death of macrophages; however, the cell death was not affected by TDAG8 deficiency. While DEX inhibited lipopolysaccharide-induced production of tumor necrosis factor-¦Á, an inflammatory cytokine, which was independent of TDAG8, at neutral pH, the glucocorticoid enhanced the acidic pH-induced inhibition of tumor necrosis factor-¦Á production in a manner dependent on TDAG8. In conclusion, the DEX-induced increase in TDAG8 expression is in part involved in the glucocorticoid-induced anti-inflammatory actions through the inhibition of inflammatory cytokine production under the acidic pH environment. On the other hand, the role of TDAG8 in the DEX-induced cell death is questionable.