PTGS2 and glomerulonephritis: This speculation is supported by our findings that PPARβ/δ was functionally expressed in human glomerular mesangial cells, where its activation and overexpression markedly enhanced basal and IL-1β-induced COX-2 expression and PGE2 production, which may accelerate glomerulonephritis by promoting the biosynthesis of the proinflammatory chemokines and cytokines responsible for the recruitment of leukocytes from circulation to the glomeruli.