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Apoptotic cell-derived factors induce arginase II expression in murine macrophages by activating ERK5/CREB

Apoptotic cell-derived factors induce arginase II expression in murine macrophages by activating ERK5/CREB,10.1007/s00018-010-0537-x,Experientia,Vera

Apoptotic cell-derived factors induce arginase II expression in murine macrophages by activating ERK5/CREB  
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Apoptotic cell (AC)-derived factors alter the physiology of macrophages (MΦs) towards a regulatory phenotype, characterized by reduced nitric oxide (NO) production. Impaired NO formation in response to AC-conditioned medium (CM) was facilitated by arginase II (ARG II) expression, which competes with inducible NO synthase for l-arginine. Here we explored signaling pathways allowing CM to upregulate ARG II in RAW264.7 MΦs. Sphingosine-1-phosphate (S1P) was required and acted synergistically with a so far unidentified factor to elicit high ARG II expression. S1P activated S1P2, since S1P2 knockdown prevented ARG II upregulation. Furthermore, ERK5 knockdown attenuated CM-mediated ARG II protein induction. CREB was implicated as shown by EMSA analysis and decoy-oligonucleotides scavenging CREB in RAW264.7 MΦs, which blocked ARG II expression. We conclude that AC-derived S1P binds to S1P2 and acts synergistically with other factors to activate ERK5 and concomitantly CREB. This signaling cascade shapes an anti-inflammatory MΦ phenotype by ARG II induction.
Journal: Experientia , vol. 68, no. 10, pp. 1815-1827, 2011
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