Fig. 7: DPI upregulates glycolysis and suppresses inflammatory responses of Kupffer cells from patients with NAFLD. | Nature Communications

Fig. 7: DPI upregulates glycolysis and suppresses inflammatory responses of Kupffer cells from patients with NAFLD.

From: Activation of GPR3-β-arrestin2-PKM2 pathway in Kupffer cells stimulates glycolysis and inhibits obesity and liver pathogenesis

Fig. 7: DPI upregulates glycolysis and suppresses inflammatory responses of Kupffer cells from patients with NAFLD.

a, b scRNAseq analysis of the liver macrophage populations. A total of 5497 macrophages based on the expression of CD14 and CD68 (clusters 5, 8, and 12 in Supplementary Fig. 10c) were subjected to clustering analysis by tSNE. A total of 7 clusters were identified (a). Each cluster was annotated based on the expression of typical markers or specific functional markers, as shown by dot plot (b). c Trajectory inference of the liver macrophages by slingshot60. d, e GO enrichment analysis of differentially expressed genes (DEGs) between C3 and C0 (d) or C3 and C1/2 (e). f, g Comparison of gene expression changes induced by DPI in primary KCs isolated from NAFLD liver biopsies. CD14+ KCs were sorted from single cell suspensions of NAFLD human liver biopsies (n = 2) and treated with DMSO or DPI (500 nM) for 24 h, followed by RNAseq to quantify gene expression. Shown are the expression changes of glycolytic genes and DAM markers (f) and GO enrichment analysis of DEGs induced by DPI in KCs (g). Orange and blue graphs in d, e, and g indicate upregulated and downregulated pathways as labeled. P values in d, e, and g were computed by Fisher’s Exact test. Source data are provided as a Source Data file.

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