Abstract
Sebaceous glands play important roles in the maintenance of the skin barrier function by secreting sebum onto the skin surface. In our study, we demonstrated that differentiated hamster sebocytes (DHS) exhibited apoptosis resistance and the loss of Ca(2+) influx against a calcium ionophore, A23187 treatment, which induced both apoptosis and Ca(2+) influx in undifferentiated hamster sebocytes (unDHS). The Fluo-3-related signal of intracellular Ca(2+) in the DHS was higher than that in unDHS and was sustained even though there was a depletion of Ca(2+) from the culture medium. Furthermore, the intracellular Ca(2+) chelator, BAPTA-AM, was found to decrease the Ca(2+) signal in the DHS, which induced apoptosis. Thus, these results provide novel evidence that the cell differentiation-dependent increase in store-operated Ca(2+) release is associated with apoptosis resistance in the DHS. Moreover, these findings should accelerate the understanding of the mechanisms of sebogenesis and/or sebum production and secretion under physiological conditions.
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