Ahn S K, Hwang S M, Jiang S J, Choi E H, Lee S H
Department of Dermatology, Yonsei University Wonju College of Medicine, Wonju, Korea.
J Invest Dermatol. 1999 Aug;113(2):189-95. doi: 10.1046/j.1523-1747.1999.00650.x.
Disruption of the epidermal permeability barrier causes an immediate loss of the calcium gradient, and barrier recovery is parallel with the restoration of the calcium gradient in the epidermis. Artificial restoration of the barrier function by occlusion with a water vapor-impermeable membrane abrogate the expected increase in lipid synthesis and retard the barrier recovery, as well as block the normalization of the epidermal calcium gradient. To clarify the long-term effects of occlusion after acute barrier perturbation, we studied the calcium distribution and epidermal keratinocytes response after occlusion with a water vapor-impermeable membrane immediately following tape stripping in the murine epidermis. Acute barrier disruption caused an immediate depletion of most calcium ions in the upper epidermis, obliterating the normal calcium gradient. When the skin barrier function was artificially corrected by occlusion, the return of calcium ions to the epidermis was blocked. After 2 h of air exposure or occlusion, the density of epidermal calcium precipitates remained negligible. The transitional cell layers appeared with occlusion, but not or negligibly with air exposure. By 6 h though, calcium precipitates could be seen, the density of the calcium precipitates with occlusion was more sparse than with air exposure. With the air exposure, the thickness of the stratum corneum had normalized and the calcium gradient nearly recovered to normal after 24 h. The longer the occlusion period, the greater was the increase of transitional cells. By 60 h of occlusion, the thickness of the stratum corneum had increased and the transitional cell layers had disappeared, in parallel with the calcium gradient which was almost normalized. These results show that prolonged occlusion of tape-stripped epidermis induced transitional cells and delayed the restoration of the epidermal calcium gradient, the stratum corneum was then restored, transitional cells having disappeared, in parallel with normalization of the epidermal calcium gradient.
表皮通透性屏障的破坏会导致钙梯度立即丧失，而屏障的恢复与表皮中钙梯度的恢复平行。用不透水蒸气的膜进行封闭人工恢复屏障功能，会消除脂质合成预期的增加并延缓屏障恢复，同时还会阻碍表皮钙梯度的正常化。为了阐明急性屏障扰动后封闭的长期影响，我们研究了在小鼠表皮进行胶带剥离后立即用不透水蒸气的膜封闭后钙的分布和表皮角质形成细胞的反应。急性屏障破坏导致上表皮中大多数钙离子立即耗尽，消除了正常的钙梯度。当通过封闭人工纠正皮肤屏障功能时，钙离子返回表皮的过程被阻断。暴露于空气或封闭2小时后，表皮钙沉淀的密度仍然可以忽略不计。封闭会出现过渡细胞层，但暴露于空气时则不会出现或仅有微不足道的过渡细胞层。不过到6小时时，可以看到钙沉淀，封闭组的钙沉淀密度比暴露于空气组更稀疏。暴露于空气后，角质层厚度已恢复正常，24小时后钙梯度几乎恢复到正常。封闭时间越长，过渡细胞增加得越多。到封闭60小时时，角质层厚度增加，过渡细胞层消失，同时钙梯度几乎恢复正常。这些结果表明，胶带剥离后的表皮长时间封闭会诱导过渡细胞并延迟表皮钙梯度的恢复，随后角质层恢复，过渡细胞消失，同时表皮钙梯度恢复正常。
