TY  - JOUR
N1  - Copyright of this article belongs to ASBMB.
ID  - open1769
UR  - http://www.jbc.org/content/early/2015/05/07/jbc.M115.638064
IS  - 30
A1  - Mahajan, Sahil
A1  - Saini, Ankita
A1  - Chandra, Vemika
A1  - Nanduri, Ravikanth
A1  - Kalra, Rashi
A1  - Bhagyaraj, Ella
A1  - Khatri, Neeraj
A1  - Gupta, Pawan
Y1  - 2015/07/24/
N2  - The orphan nuclear receptor Nr4a2 is known to modulate both inflammatory and metabolic processes, but the mechanism by which it regulates innate inflammatory homeostasis has not been adequately addressed. This study shows that exposure to ligands for Toll-like receptors (TLRs) robustly induces Nr4a2 and that this induction is tightly regulated by the PI3K-Akt signaling axis. Interestingly, exogenous expression of Nr4a2 in macrophages leads to their alternative phenotype with induction of genes that are prototypical M2 markers. Moreover, Nr4a2 transcriptionally activates arginase 1 expression by directly binding to its promoter. Adoptive transfer experiments revealed that increased survival of animals in endotoxin-induced sepsis is Nr4a2-dependent. Thus our data identify a previously unknown role for Nr4a2 in the regulation of macrophage polarization.
PB  - ASBMB
JF  - The Journal of biological chemistry
VL  - 290
KW  - gene transcription; inflammation;macrophage ;
nuclear receptor
sepsis
Arginase 1;
SN  - 1083-351X
TI  - Nuclear Receptor Nr4a2 Promotes Alternative Polarization of Macrophages and Confers Protection in Sepsis.
SP  - 18304
EP  - 14
ER  -