Fig. 3: Primary human hepatocytes from a donor homozygous for the 186T allele had lower PSD3 protein and intracellular lipid levels compared with homozygous 186L hepatocytes. Primary human hepatocytes from donors homozygous for 186L or 186T, were cultured in 2D. | Nature Metabolism

Fig. 3: Primary human hepatocytes from a donor homozygous for the 186T allele had lower PSD3 protein and intracellular lipid levels compared with homozygous 186L hepatocytes. Primary human hepatocytes from donors homozygous for 186L or 186T, were cultured in 2D.

From: PSD3 downregulation confers protection against fatty liver disease

Fig. 3: Primary human hepatocytes from a donor homozygous for the 186T allele had lower PSD3 protein and intracellular lipid levels compared with homozygous 186L hepatocytes. Primary human hepatocytes from donors homozygous for 186L or 186T, were cultured in 2D.

a, Intracellular neutral fat content visualized by ORO staining and quantified by Biopix iQ software v.2.3.1. Data are presented as mean and s.d. of the reported independent experiments (n = 5). Two-sided P value was calculated by Mann–Whitney non-parametric test. b, Cells were cultured in serum-free regular medium supplemented with 2% FBS, 10 µM OA or 25 µM OA for 48 h. Immunoblotting was performed with total cell lysates to detect PSD3 (NCBI: NP_056125, 1,047 amino acids) using a custom antibody. The bar graph shows the relative PSD3 amount calculated as PSD3/calnexin (CNX). c, Key genes involved in lipid metabolism that were differentially expressed between donors homozygous for 186T versus 186L obtained with RNA-seq. Data are presented as log2(fold change) in expression and –log10(P value) adjusted using the Benjamini and Hochberg’s approach for controlling the FDR. RU, relative units; VLDL, very low-density lipoprotein. Red Triglyceride synthesis; yellow VLDL secretion; blue Fatty acid oxidation; black cholesterol metabolism.

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