RGS2 is a negative regulator of STAT3-mediated Nox1 expression
- RGS2 is a negative regulator of STAT3-mediated Nox1 expression
- 백석환; 이형경; 박대원; 배준호[배준호]; 김형준[김형준]; 신동구; 박종선; 이진구[이진구]; 이성중[이성중]; 배외식[배외식]
- OXIDASE 1 EXPRESSION; FOAM CELL-FORMATION; TOLL-LIKE RECEPTORS; BLOOD-PRESSURE; ANGIOTENSIN-II; HYPERTENSIVE PATIENTS; NADPH OXIDASES; PROTEINS; LIPOPOLYSACCHARIDE; INFECTION
- Issue Date
- ELSEVIER SCIENCE INC
- CELLULAR SIGNALLING, v.24, no.3, pp.803 - 809
- NADPH oxidase 1 (Nox1) is essential for reactive oxygen species production in the innate immune responses mediated by toll-like receptor (TLR), but the mechanism regulating its expression remains uncertain. Here, we find that Nox1 induction is TLR2-dependent, but independent of myeloid differentiation primary response gene 88 (MyD88). We demonstrate the capacity of signal transducer and activator of transcription 3 (STAT3) to activate Nox1's transcription, as well as cooperative regulation by Janus kinase 1 and 3 (JAK1 and JAK3). We find that regulator of G-protein signaling 2 (RGS2) inhibits STAT3-mediated Nox1 transcription, and can itself be repressed by TLR2; Nox1 induction upon RGS2 down-regulation is controlled by protein kinase C-eta (PKC-eta) and phospholipase D2 (PLD2). A GFP-tagged version of RGS2 concentrates in the nucleus; RGS2 additionally directly binds STAT3 to regulate its transcriptional activity through TLR2 stimulation. Cumulatively, these results suggest that TLR2 signaling enhances Nox1 expression through the JAK1/3-STAT3 pathway, and that RGS2, through its regulation by the PKC-eta/PLD2 pathway, represses STAT3's transcriptional activation of Nox1. (C) 2011 Published by Elsevier Inc.
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