Fig. 2

Endocytosis of apoA-V in both normal and lipid-accumulated HL-1 cells. A Subcellular localization of apoA-V detected by fluorescence and confocal microscopy. ApoA-V was localized within HL-1 cells with (A-c) or without (A-b) lipid accumulation (scale bar: 25 μm; nuclei: blue; apoA-V: green; A-a: normal HL-1 cells without apoA-V). B The [¹²⁵I] radioactivity detection results of [¹²⁵I]-apoA-V in HL-1 cells. In normal HL-1 cells, ~ 20% of [¹²⁵I]-apoA-V uptake remained intracellular over a 24 h chase period, while 80% was degraded (B-a); however, in HL-1 cells with lipid accumulation, ~ 44% of [¹²⁵I]-apoA-V uptake remained intracellular, and 56% was degraded over a 24 h chase period (B-b). C Western blot analysis of the uptake of apoA-V by HL-1 cells. β-actin served as a loading control