Mauro T, Bench G, Sidderas-Haddad E, Feingold K, Elias P, Cullander C
Dermatology Service, Veterans Affairs Medical Center, San Francisco, California 94121, USA.
J Invest Dermatol. 1998 Dec;111(6):1198-201. doi: 10.1046/j.1523-1747.1998.00421.x.
Epidermal permeability barrier homeostasis requires the delivery of lipids and hydrolytic enzymes by lamellar body exocytosis from the uppermost granular cells, a process that is upregulated following barrier disruption. As lamellar body secretion is controlled by ionic concentrations, especially Ca2+ and K+, we used a quantitative technique, microbeam proton-induced X-ray emission, to measure Ca2+, K+, Cl-, and P concentrations before and after acute barrier perturbation by acetone applications. We found a steep gradient of Ca2+ in normal tissue, peaking in the outer stratum granulosum, which disappeared after barrier disruption, and partially reformed as the barrier recovered. A similar gradient, peaking somewhat lower in the epidermis (i.e., at the stratum granulosum-stratum corneum interface), was found for K+. Epidermal concentrations of K+ also decreased after barrier abrogation, although to a lesser extent than Ca2+. In contrast, P and Cl- demonstrated distribution gradients at baseline, which remained unchanged after barrier disruption. These studies quantitate the levels of Ca2+, K+, Cl-, and P within specific epidermal cell layers at baseline, and in relation to changes in permeability barrier integrity. Ca2+ and K+, but not Cl- or P, decrease after barrier disruption, consistent with these two ion's role in barrier repair.
表皮通透屏障的稳态需要最上层颗粒细胞通过板层小体胞吐作用来输送脂质和水解酶，这一过程在屏障破坏后会上调。由于板层小体的分泌受离子浓度控制，尤其是Ca2+和K+，我们采用了一种定量技术——微束质子诱导X射线发射，来测量丙酮急性破坏屏障前后Ca2+、K+、Cl-和P的浓度。我们发现在正常组织中Ca2+存在陡峭的梯度，在颗粒层外层达到峰值，屏障破坏后该梯度消失，并在屏障恢复时部分重新形成。K+也有类似的梯度，在表皮中的峰值略低（即位于颗粒层-角质层界面）。屏障废除后表皮中K+的浓度也降低了，尽管程度小于Ca2+。相比之下，P和Cl-在基线时呈现分布梯度，屏障破坏后保持不变。这些研究定量了基线时特定表皮细胞层内Ca2+、K+、Cl-和P的水平，以及与通透屏障完整性变化的关系。屏障破坏后Ca2+和K+（而非Cl-或P）减少，这与这两种离子在屏障修复中的作用一致。
