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KMID : 1161520160200010001
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Animal Cells and Systems
2016 Volume.20 No. 1 p.1 ~ p.6
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Glucocorticoid-mediated anti-inflammatory effect through NFκB is preserved in the absence of Dexras1
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Yong Ji-Hyun
Seok Jo-Woon
Yu Jung-Hwan
Choi Yoon-Jeong
Song Su-Jin
Kim A-Ra
Kim Hyo-Jung
Kim Jae-Woo
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Abstract
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Glucocorticoids effectively mediate the resolution of inflammation, but long-term use of glucocorticoids inevitably causes metabolic side effects. However, it is unknown if metabolic effectors such as Dexras1, a dexamethasone-stimulated protein, play a role in the anti-inflammatory outcome of dexamethasone. Here, we demonstrate that Dexras1 is required for the dexamethasone-induced upregulation of annexin A1 expression, but is not involved in the reduction of inflammation as evidenced by decreased pro-inflammatory parameters. In the absence of Dexras1, lipopolysaccharide (LPS)-induced interleukin-6 expression was suppressed when murine macrophage RAW264.7 cells were treated with dexamethasone. Similar observations were made in the blood of Dexras1 knockout mice. Furthermore, dexamethasone suppressed the LPS-stimulated increase of NFκB-p65 in both control and Dexras1-absent RAW264.7 cells. Interestingly, depletion of Dexras1 resulted in the loss of pERK production. These results suggest that Dexras1 is involved primarily in the metabolic side effects and its inhibition preserves the anti-inflammatory action of glucocorticoids. Thus, the inhibition of Dexras1 will be an excellent target for reducing steroid-induced side effects.
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KEYWORD
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Dexras1, glucocorticoid, anti-inflammatory effects, dexamethasone, NFκB, IL-6
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