Localization of calcium in murine epidermis following disruption and repair of the permeability barrier

Summary

Perturbation of the cutaneous permeability barrier results in rapid secretion of epidermal lamellar bodies, and synthesis and secretion of new lamellar bodies leading to barrier repair. Since external Ca²⁺ significantly impedes the repair response, we applied ion capture cytochemistry to localize Ca²⁺ in murine epidermis following barrier disruption. In controls, the numbers of Ca²⁺ precipitates in the basal layer were small, increasing suprabasally and reaching the highest density in the stratum granulosum. Barrier disruption with acetone produced an immediate, marked decrease in Ca²⁺ in the stratum granulosum, accompanied by secretion of lamellar bodies. Loss of this pattern of Ca²⁺ distribution was associated with the appearance of large Ca²⁺ aggregates within the intercellular spaces of the stratum corneum. The Ca²⁺-containing precipitates progressively reappeared in parallel with barrier recovery over 24 h. Disruption of the barrier with tape stripping also resulted in loss of Ca²⁺ from the nucleated layers of the epidermis, but small foci persisted where the stratum corneum was not removed; in these sites the Ca²⁺ distribution did not change and accelerated secretion of lamellar bodies was not observed. Following acetone-induced barrier disruption and immersion in isoosmolar sucrose, the epidermal Ca²⁺ gradient did not return, and both lamellar body secretion and barrier recovery occurred. However, with immersion in isoosmolar sucrose plus Ca²⁺, the epidermal Ca²⁺ reservoir was replenished, and both secretion of lamellar bodies and barrier recovery were impeded. These results demonstrate that barrier disruption results in loss of the epidermal Ca²⁺ reservoir, which may be the signal that initiates lamellar body secretion leading to barrier repair.