RGS10 differentially modulates NFκB subunit transcription and inflammatory cytokine profiles in peritoneal macrophages.

Abstract

Regulator of G-protein signaling 10 (RGS10) has been shown to regulate multiple inflammatory pathways relevant to disease pathogenesis. Of particular importance is the ability of RGS10 to negatively regulate the NFkB pathway, a prominent pro-inflammatory pathway implicated in multiple inflammatory disease phenotypes. However, the exact mechanism by which RGS10 regulates NFkB is unknown. Considering that RGS10 translocates into the nucleus upon stimulation, we hypothesize that RGS10 may regulate NFKB through transcription. To determine whether RGS10 mediates NFkB transcription, we stimulated RGS10 KO and B6 peritoneal macrophages and collected cell lysate over 24 hours to assess transcript levels of NFkB and related proinflammatory cytokines. Here we found that RGS10 differentially regulates the transcription of N{kappa}KB subunits and NF{kappa}B-dependent cytokines. Further studies are warranted to understand the potential role of RGS10 in transcriptional regulation of inflammatory states.