Structural and biochemical basis for the UVB-induced alterations in epidermal barrier function
Structural and biochemical basis for the UVB-induced alterations in epidermal barrier function
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DOI：
10.1111/j.1600-0781.1997.tb00214.x
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发表时间：
1997-08-01
影响因子：
2.6
通讯作者：
Elias, PM
中科院分区：
文献类型：
--
作者：
Holleran, WM;Uchida, Y;Elias, PM
紫外线（UVR）可诱导无数皮肤变化，包括较高剂量的渗透屏障延迟破坏。为了研究WE诱导的屏障改变的基础，我们评估了表皮板层体分泌系统在不同的时间点之前和之后的屏障破坏与一个单一的高剂量的UVB（7.5 MED）小鼠表皮。形态学数据与表皮增殖和脂质合成的变化相关，表明板层体的产生。UVB照射后24小时，角质层（SC）是正常的，但在颗粒层（SG）ISC界面的正下方存在一层异常的空泡化和板层体（LB）缺陷细胞。紧接着这条受损细胞带，存在含有完整LB的正常角质形成细胞。72小时，伴随着出现的屏障异常，广泛受损的细胞持续在SC/SG接口，和异常板层膜结构出现在较低的SC。上层棘层（SS）和较低的SG细胞出现正常，与LB的数量增加。屏障异常仍然存在，在96小时，在较低的SC间隙与膜异常，但多达四个正常出现，subjunctional SG细胞层存在。到120小时，加速LB形成和早熟LB挤出发生在整个增厚的SG;正常的层状膜存在于较低的SC和屏障恢复几乎是完全的。然而，主要屏障脂质种类的表皮合成（即，胆固醇，脂肪酸和神经酰胺，包括酰基神经酰胺）在24和48小时减少或不变，在暴露于UVB后72小时显著增加。因此，急性UVB暴露后渗透性屏障的延迟破坏是由于板层体功能不全（即，在SG/SC界面处的损坏的）细胞。随后，屏障的快速恢复反过来又是由皮下未受损的SS/SG细胞的代偿性增生引起的，产生了LB数量和含量的增加。这些结果强调了致密层在介导屏障功能中的关键作用，并表明UV暴露的有益治疗效果可能是由于增强的脂质产生和屏障再生。
Ultraviolet light (UVR) induces a myriad of cutaneous changes, including delayed disruption of the permeability barrier with higher doses. To investigate the basis for the WE-induced barrier alteration, we assessed the epidermal lamellar body secretory system at various time points before and after barrier disruption with a single high dose of UVB (7.5 MED) to murine epidermis. Morphological data were correlated with changes in epidermal proliferation and lipid synthesis, indicative of lamellar body generation. Twenty-four hours following UVB, the stratum corneum (SC) is normal, but a layer of abnormal, vacuolated, and lamellar body (LB)-deficient cells is present, immediately beneath the stratum granulosum (SG)ISC interface. Immediately subjacent to this band of damaged cells, normal keratinocytes that contain intact LBs are present. By 72 h, concomitant with the appearance of a barrier abnormality, extensively damaged cells persist at the SC/SG interface, and abnormal lamellar membrane structures appear in the lower SC. Upper stratum spinosum (SS) and lower SG cells appear normal, with increased numbers of LBs. A barrier abnormality is still present at 96 h, in association with membrane abnormarities in the lower SC interstices, but up to four normal-appearing, subjacent SG cell layers are present. By 120 h, accelerated LB formation and precocious LB extrusion occur throughout the thickened SG; normal lamellar membranes are present in the lower SC; and barrier recovery is almost complete. Whereas, epidermal synthesis of the major barrier lipid species (i.e., cholesterol, fatty acids, and ceramides, including acylceramides) is reduced or unchanged at 24 and 48 h, it increases significantly 72 h after exposure to UVB. Therefore, the delayed disruption of the permeability barrier following acute UVB exposure results from the arrival of a band of lamellar body-incompetent (i.e., damaged) cells at the SG/SC interface. The subsequent, rapid recovery of the barrier, in turn, results from compensatory hyperplasia of subjacent, undamaged SS/SG cells, generating increased numbers and contents of LB. These results underscore the critical role of the stratum compactum in mediating barrier function, and suggest that beneficial therapeutic effects of UV exposure may be due to enhanced lipid production and barrier regeneration.