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. 2025 Aug 28;5(1):100774. doi: 10.1016/j.gastha.2025.100774

Figure 3.

Figure 3

TM6SF2 E167K-edited HLC exacerbates steatosis phenotype with impaired VLDL secretion. (A) Representative images of genome-edited HLCs ± AALAT treatment, stained for lipid droplets and nuclei. Lipid droplets were stained with BODIPY 493/503, and nuclei were counterstained with Hoechst 33,342. (B) The intensity ratio of BODIPY to nuclei in genome-edited HLCs was quantified (∗∗∗P < .001, ∗P < .05, Tukey’s post hoc tests). (C) The TG content of genome-edited HLCs was analyzed (∗∗∗P < .001, Tukey’s post hoc-tests). (D) ApoB100 secreted by genome-edited HLCs into fresh culture medium was measured at three time points (n = 4 per a group, ∗P < .05, Student’s t-test). (E) Lipoproteins were fractionated from the culture supernatants of EE or KK HLCs, and ApoB100 in each fraction was analyzed by ELISA (n = 4 per a group, ∗∗P < .01, ∗P < .05, Student’s t-test). (F) The number of double bonds in PC of EE or KK HLCs was examined by using LC-MS/MS (∗∗P < .01, Student’s t-test). (G) Fatty acid content in PC of EE or KK HLCs was analyzed (∗∗P < .01, Student’s t-test). (H) Schematic overview of the TG composition analysis is shown. Lipids were extracted from the culture supernatant and cell lysate, and analyzed using LC-MS/MS. (I) Principal component analysis was performed on the relative abundance of TG species inside and outside of EE or KK HLCs. (J) Heat map shows the changes in the proportion of TG species in KK HLC (∗P < .05, Student’s t-test). All data represent mean ± SD.