Induction of selected lipid metabolic enzymes and differentiation-linked structural proteins by air exposure in fetal rat skin explants.
Induction of selected lipid metabolic enzymes and differentiation-linked structural proteins by air exposure in fetal rat skin explants.
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通过胎鼠皮肤外植体暴露于空气中诱导选定的脂质代谢酶和分化相关结构蛋白。
DOI：
10.1046/j.1523-1747.1999.00511.x
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Feingold,KR
中科院分区：
文献类型：
--
作者：
Komuves,LG;Hanley,K;Jiang,Y;Katagiri,C;Elias,PM;Williams,ML;Feingold,KR
早产儿的表皮通透性屏障在出生后迅速成熟。以前的研究表明，空气暴露可能有助于这种加速，因为：(I)当胎鼠皮肤外植体在空气-介质界面孵化时，结构和功能成熟的屏障的形成加速，以及(Ii)用不透水的膜封闭阻止了这种加速。为了进一步探讨空气暴露对表皮屏障个体发生的影响，我们比较了暴露于空气中的胎鼠皮肤组织中几种脂代谢关键酶的活性和表皮分化蛋白标记物的基因表达。胆固醇(HMG CoA还原酶)和神经酰胺(丝氨酸棕榈酰转移酶)合成的限速酶不受影响。相比之下，分别负责合成葡萄糖神经酰胺和胆固醇硫酸盐的葡萄糖神经酰胺合成酶和胆固醇磺基转移酶活性的正常发育增加，在空气暴露下进一步加速。此外，屏障成熟的最后阶段和正常角质层功能所必需的两种酶--β-葡萄糖脑苷酶和类固醇硫酸酯酶--也随着空气暴露而增加，前者将葡萄糖神经酰胺转化为神经酰胺，后者可使胆固醇硫酸盐脱除。此外，丝状蛋白和氯化蛋白的mRNA水平以及细丝蛋白、氯化蛋白和总蛋白的水平都随着空气暴露的增加而增加。最后，用水不透膜封闭可以阻止空气暴露引起的脂酶活性的增加，以及氯化蛋白、丝状蛋白和总蛋白的表达。因此，空气暴露可刺激胎儿表皮中某些脂代谢酶和关键结构蛋白的基因表达，为空气诱导早产儿通透性屏障成熟的加速提供生化基础。
The epidermal permeability barrier of premature infants matures rapidly following birth. Previous studies suggest that air exposure could contribute to this acceleration, because: (i) development of a structurally and functionally mature barrier accelerates when fetal rat skin explants are incubated at an air–medium interface, and (ii) occlusion with a water-impermeable membrane prevents this acceleration. To investigate further the effects of air exposure on epidermal barrier ontogenesis, we compared the activities of several key enzymes of lipid metabolism and gene expression of protein markers of epidermal differentiation in fetal rat skin explants grown immersedversusair exposed. The rate-limiting enzymes of cholesterol (HMG CoA reductase) and ceramide (serine palmitoyl transferase) synthesis were not affected. In contrast, the normal developmental increases in activities of glucosylceramide synthase and cholesterol sulfotransferase, responsible for the synthesis of glucosylceramides and cholesterol sulfate, respectively, were accelerated further by air exposure. Additionally, two enzymes required for the final stages of barrier maturation and essential for normal stratum corneum function, β-glucocerebrosidase, which converts glucosylceramide to ceramide, and steroid sulfatase, which desulfates cholesterol sulfate, also increased with air exposure. Furthermore, filaggrin and loricrin mRNA levels, and filaggrin, loricrin, and involucrin protein levels all increased with air exposure. Finally, occlusion with a water-impermeable membrane prevented both the air-exposure-induced increase in lipid enzyme activity, and the expression of loricrin, filaggrin, and involucrin. Thus, air exposure stimulates selected lipid metabolic enzymes and the gene expression of key structural proteins in fetal epidermis, providing a biochemical basis for air-induced acceleration of permeability barrier maturation in premature infants.