ISSN:
1432-0878
Keywords:
Epidermis
;
Permeability
;
Calcium ions
;
Ionic localization
;
Mouse (hr/hr)
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
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.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00645052
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