RGS5 and atherosclerosis: In the CNS, mice lacking Rgs5 selectively in astrocytes displayed a marked attenuation of LPS-induced increases in pro-inflammatory mediator levels; whereas, in the peripheral tissues/cells, such as vascular endothelial cells, RGS5 has a distinct function, as shown by the loss of Rgs5 exacerbating disease severity in an animal model of atherosclerosis partially through increased inflammatory mediator expression in vessels [67, 68].