AIM: Senescence marker protein-30 (SMP30)/gluconolactonase (GNL) is an age-associated protein in that its presence decreases with aging. Here, we used immunohistochemical analysis to investigate the changes of SMP30/GNL in individual cells of the liver from progressively aged mice. METHODS: Male C57BL/6 strain mice at 1, 3, 6, 12, 24 and 30 months-of-age were the source of hepatic cells used to detect SMP30/GNL. Liver sections from these mice were subjected to immunohistochemical staining with anti-SMP30/GNL antibody. For immunofluorescent staining, primary cultured hepatocytes from mice at various ages were stained with SMP30/GNL and albumin. RESULTS: In liver cells from mice of all ages, SMP30/GNL staining appeared in some but not all parenchymal cells, and localized in both the nuclei and cytoplasm. Moreover, SMP30/GNL-positive staining of parenchymal cells was present only around central vein areas, but not at sites of portal veins. Furthermore, the number of SMP30/GNL-positive cells increased as mice aged from 1 to 12 months, then decreased from the 12th to 24th month. Results were similar in primary cultured hepatocytes from mice of various ages. CONCLUSIONS: SMP30/GNL-positive cells localized mainly around the central veins in the livers of mice and decreased numerically with aging, although there was no age-related change in counts of albumin-positive cells. SMP30/GNL protein occupied the nuclei and cytoplasm. Therefore, nuclear SMP30/GNL protein might be a regulatory factor specific for genes whose expression governs transcription and the aging process.
AIM: Senescence marker protein-30 (SMP30)/gluconolactonase (GNL) is an age-associated protein in that its presence decreases with aging. Here, we used immunohistochemical analysis to investigate the changes of SMP30/GNL in individual cells of the liver from progressively aged mice. METHODS: Male C57BL/6 strain mice at 1, 3, 6, 12, 24 and 30 months-of-age were the source of hepatic cells used to detect SMP30/GNL. Liver sections from these mice were subjected to immunohistochemical staining with anti-SMP30/GNL antibody. For immunofluorescent staining, primary cultured hepatocytes from mice at various ages were stained with SMP30/GNL and albumin. RESULTS: In liver cells from mice of all ages, SMP30/GNL staining appeared in some but not all parenchymal cells, and localized in both the nuclei and cytoplasm. Moreover, SMP30/GNL-positive staining of parenchymal cells was present only around central vein areas, but not at sites of portal veins. Furthermore, the number of SMP30/GNL-positive cells increased as mice aged from 1 to 12 months, then decreased from the 12th to 24th month. Results were similar in primary cultured hepatocytes from mice of various ages. CONCLUSIONS:SMP30/GNL-positive cells localized mainly around the central veins in the livers of mice and decreased numerically with aging, although there was no age-related change in counts of albumin-positive cells. SMP30/GNL protein occupied the nuclei and cytoplasm. Therefore, nuclear SMP30/GNL protein might be a regulatory factor specific for genes whose expression governs transcription and the aging process.