Adenosine A2A receptor signaling attenuates LPS-induced pro-inflammatory cytokine formation of mouse macrophages by inducing the expression of DUSP1
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- 作者：Krisztina Kö ; rö ; ské ; nyi ; Beá ; ta Kiss ; Zsuzsa Szondy ; szondy@med.unideb.hu" class="auth_mail" title="E-mail the corresponding author
- 关键词：A2AR ; adenosine A2A receptor ; AP-1 ; activator protein 1 ; BLC ; B-lymphocyte chemoattractant ; BMDM ; bone marrow derived macrophage ; CREB ; cAMP response element-binding protein ; DUSP1 ; dual specific phosphatase ; Epac ; exchange protein activated by cAMP ; ERK ; extracellular signal-regulated kinase ; HPRT ; hypoxanthine-guanine phosphoribosyltransferase ; hsp ; heat shock protein ; IFN ; interferon ; IKK ; IκB kinase ; IP-10 ; γ interferon-inducible cytokine ; IκB ; inhibitor of κ light chain gene enhancer in B c
- 刊名：Biochimica et Biophysica Acta (BBA)-Molecular Cell Research
- 出版年：2016
- 出版时间：July 2016
- 年：2016
- 卷：1863
- 期：7
- 页码：1461-1471
- 全文大小：2789 K
文摘
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LPS stimulation of A2AR null macrophages results in a higher pro-inflammatory response.
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Loss of A2ARs does not affect the LPS-induced NF-κB signaling pathway in macrophages.
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Loss of A2ARs results in higher basal and LPS-induced MAPK phosphorylation.
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A2AR signaling does not decrease MKK activation, but maintains high DUSP1 expression.
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DUSP1 levels are regulated by A2ARs via the adenylate cyclase signaling pathway.