Fig. 2.

PlsEtn deficiency aggravates hepatic steatosis via p75NTR. (A) AML12 cells were transfected with shGNPAT or scrambled control (shCTRL1) and subsequently exposed to 400 μM PA for an additional 48 h. Lipid droplets accumulation within the AML12 cells were determined by Oil-red O staining and quantified at 500 nm. (B) Representative Western blot indicating the protein expression of p75NTR and lipolysis related genes in AML12 cells treated with shGNPAT. (C) AML12 cells were transfected with shp75NTR or scrambled control (shCTRL2) and subsequently exposed to 400 μM PA for an additional 48 h. Lipid droplets accumulation were determined by Oil-red O staining and quantified at 500 nm. (D) 6-week old mice was used to develop hepatic steatosis under high fat high fructose diet and treated with recombinant AAV virus of shGnpat. (E) Photomicrographs depicting the liver from AAV-shGnpat-treated and HFSD-fed mice (n = 5 mice/group) stained for H&E and Oil red O. (F) Representative Western blot indicating the protein expression of p75NTR and lipolysis related genes in AAV-shGnpat-treated and HFSD-fed mice. (G) Hepatic triglyceride levels in AAV-shGnpat-treated and HFSD-fed mice. (H) Hepatic total cholesterol in AAV-shGnpat-treated and HFSD-fed mice. (I) Representative Western blot indicating the protein expression of p75NTR and lipolysis related genes in AML12 cells treated with shp75NTR. Statistical significance was determined by Student's t-test, *p < 0.05, **p < 0.01 vs scrambled control. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)