The word “aging” has two meanings. One is cellular senescence, which shows cellular hypertrophy, growth arrest, and telomere shortening. Another is human aging, which shows organ dysfunction. For long term maintenance of normal biological functions, it is important to clarify the relationship between cellular senescence and human aging.
It is well known that glycans have various functions, such as cellular discrimination and immune response. Therefore, glycans can be potential biomarkers for physiological conditions. In our previous studies, we investigated the alterations in cell surface glycans in human diploid fibroblasts derived from differently aged skin using the lectin microarray and showed that sialylated glycans on the surface of aging cells gradually decreased with cellular senescence. Moreover, both fetal- and elderly-derived cells exhibited a sequential decrease in some types of sialylated glycans.
Conversely, the details of the intracellular glycans are unclear. Thus, we investigated the alterations in intracellular glycans with methods like those used for cell surface analysis. As a result, we showed that intracellular glycans barely changed with cellular senescence. The ratio of increasing sialylated glycoproteins in the fetal-derived cells showed cellular senescence similar to that of the elderly-derived cells. Consequently, these results suggested that the alterations in the ratio between intracellular and cell surface glycans with cellular senescence contribute to human aging.
Our findings could be useful in the characterization of biomarkers of aging or in providing valuable information about functional age.