Fig. 2
From: Macrophage-derived MCPIP1 mediates silica-induced pulmonary fibrosis via autophagy
SiO2 induced cell apoptosis via autophagy. a Representative western blot showing the effects of RNAi targeting MCPIP1 on BECN and LC3B expression induced by SiO2 (50 μg/cm2) treatment for 24 h. b Densitometric analyses of five separate experiments suggested that SiO2-induced BECN and LC3B expression was attenuated by RNAi targeting MCPIP1. *p < 0.05 vs the corresponding control group; #p < 0.05 vs the corresponding SiO2 group. c Representative images showing the effect of RNAi targeting MCPIP1 on the SiO2-induced formation of RFP- and GFP-MAP1LC3 puncta at 24 h following SiO2 treatment. Scale bar = 10 μm. d Quantification of the RFP- and GFP- MAP1LC3 puncta demonstrating that SiO2-induced autophagy was attenuated by RNAi targeting MCPIP1. *p < 0.05 vs the control group; # p < 0.05 vs the SiO2 group. e Quantification of RFP-MAP1LC3 puncta and RFP- and GFP-colocalized puncta demonstrating autophagic flux induced by SiO2 was attenuated by RNAi targeting MCPIP1. *p < 0.05 vs the control group; #p < 0.05 vs the SiO2 group. f Representative western blot showing the effects of RNAi targeting MCPIP1 on SiO2-induced p53 expression. g Densitometric analyses of five separate experiments suggested that SiO2-induced p53 expression was attenuated by RNAi targeting MCPIP1. *p < 0.05 vs the control group; # p < 0.05 vs the SiO2 group. Whole cell lysates immunoprecipitated for p53 (h) or MCPIP1 (i) were then immunoblotted for MCPIP1 or p53, respectively, to determine the interaction between MCPIP1 and p53 after SiO2 exposure; IgG was used as an immunoprecipitation control. IP = immunoprecipitation; IB = immunoblot