FIGURE 8. Intralobular zonal gradient of vitamin A storage in HSCs. The zonal gradient of vitamin A storage is expressed as a symmetric biphasic profile with a peak at zone III and a downward slope toward zone V. Characteristically, the area of lipoid droplets in zone V is slightly smaller than that in zone I. Graphs were plotted with the mean value, depicting three animal species: polar bear (#), Arctic fox (A), and rat (♦).
in the PC-enriched fraction were SCs which adhered to PCs. At 3 days after PHx, in addition to desmin staining, isolated SCs were also positive for BrdU and a-SMA, and formed clusters suggesting that these HSCs were activated. At 3 days after PHx, SCs in the SC fraction were only positive for desmin, which indicated that adherence to PCs is required for HSC activation. Thus, these data suggest that HSCs are activated by adhering to PCs during the early phase of hepatic regeneration.
As mentioned earlier, under physiological conditions, HSCs within liver lobules store about 80% of the total body vitamin A in lipid droplets in their cytoplasm, and these cells show zonal heterogeneity in terms of vitamin A-storing capacity (Figs. 7 and 8). The status of vitamin A storage in SCs in the liver regeneration was examined (Higashi et al., 2005b). Morphometry at the electron microscopic level, fluorescence microscopy for vitamin A autofluorescence, and immunofluorescence microscopy for desmin and a-SMA were performed on sections of liver from rats at various times after the animal had been subjected to 70% PHx.
Under the electron microscope, the mean area of vitamin A-storing lipid droplets per HSC gradually decreased toward 3 days after PHx, and then returned to normal within 14 days after it. However, the heterogeneity of vitamin A-storing lipid droplet area per HSC within the hepatic lobule disappeared after PHx and did not return to normal by 14 days thereafter, even though the liver volume had returned to normal.
These results suggest that HSCs alter their vitamin A-storing capacity during liver regeneration and that the recovery of vitamin A homeostasis requires a much longer time than that for liver volume.
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