Fig. 8: Effects of overexpression and knockdown of Nprl3 on ARRB-mediated microglia inflammation.
From: Opposing functions of β-arrestin 1 and 2 in Parkinson’s disease via microglia inflammation and Nprl3
Inflammatory gene expression in microglia from WT and ARRB knockout mice after transfection with either NPRL3 for 24 (a) or Nprl3 siRNA for 48 h (b). Activation of p65 (c, d, g and h) and STAT1 (e, f, i and j) in microglia after Nprl3 overexpression (c–f) or knockdown (g–j) as above. k A schematic diagram showing the opposite roles of ARRB1 and ARRB2 in microglia-mediated inflammation and DA neuron degeneration via regulating Nprl3 and the inflammatory STAT1 and NF-κB pathways (see text for details). +, stimulatory; −, inhibitory. Quantitative data are mean ± s.e. (n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001.
