Ishida-Yamamoto A, Iizuka H, Manabe M, O'Guin W M, Hohl D, Kartasova T, Kuroki T, Roop D R, Eady R A
Department of Cell Pathology, St. John's Institute of Dermatology, St. Thomas's Hospital, London, UK.
Arch Dermatol Res. 1995;287(8):705-11. doi: 10.1007/BF01105793.
Epidermolytic hyperkeratosis (EH) is a genetic disorder of keratins associated with epidermal differentiation. Affected individuals carry gene mutations for conserved sequences of keratins K1 or K10. The structural alterations of tonofilaments in EH seem to be a direct consequence of the keratin gene mutations. EH epidermis, however, shows many other unexplained abnormalities including acanthosis, hypergranulosis, and hyperkeratosis. To further elucidate the pathogenetic mechanism of EH, we studied distribution patterns of other keratinization-associated molecules including involucrin, small proline-rich protein (SPRR) 1, loricrin and trichohyalin in the skin of four patients by light and electron microscopic immunohistochemistry in conjunction with conventional transmission electron microscopy. The middle to upper epidermal cells showed moderate to strong immunoreactivities to involucrin, SPRR1 and loricrin antibodies. Both intracellular staining and cell peripheral staining was seen for involucrin and SPRR1 antibodies. Loricrin labelling was prematurely associated with the plasma membrane of granular cells, possibly relating to abnormal keratin filament aggregation and cellular vacuolization. Some loricrin labelling was localized on the keratin aggregates, suggesting intermolecular associations between keratin and loricrin. Trichohyalin, hardly detectable in normal epidermis, was present in some granular and cornified cells in EH in association with keratin filaments, suggesting that it may function as an intermediate filament-associated protein. While cornified cell envelopes were intensely labelled only with loricrin antibodies in normal skin, they were immunoreactive to involucrin, SPRR1 and loricrin antibodies in EH. Sequential change in electron density of the cornified cell envelopes, a constant feature in normal skin, was often absent in EH. These results suggest an altered assembly process of cornified cell envelopes in EH.
表皮松解性角化过度(EH)是一种与表皮分化相关的角蛋白遗传性疾病。受影响个体携带角蛋白K1或K10保守序列的基因突变。EH中张力丝的结构改变似乎是角蛋白基因突变的直接后果。然而,EH表皮显示出许多其他无法解释的异常,包括棘层肥厚、颗粒层增厚和角化过度。为了进一步阐明EH的发病机制,我们通过光镜和电镜免疫组织化学结合传统透射电子显微镜,研究了4例患者皮肤中其他与角质化相关分子的分布模式,这些分子包括内披蛋白、富含脯氨酸的小蛋白(SPRR)1、兜甲蛋白和毛透明蛋白。表皮中上部细胞对内披蛋白、SPRR1和兜甲蛋白抗体呈中度至强免疫反应。内披蛋白和SPRR1抗体可见细胞内染色和细胞周边染色。兜甲蛋白标记过早地与颗粒细胞的质膜相关,这可能与异常的角蛋白丝聚集和细胞空泡化有关。一些兜甲蛋白标记定位于角蛋白聚集体上,表明角蛋白和兜甲蛋白之间存在分子间关联。毛透明蛋白在正常表皮中几乎检测不到,在EH的一些颗粒细胞和角质形成细胞中与角蛋白丝相关存在,提示它可能作为一种中间丝相关蛋白发挥作用。在正常皮肤中,角质化包膜仅用兜甲蛋白抗体强烈标记,而在EH中它们对内披蛋白、SPRR1和兜甲蛋白抗体有免疫反应。正常皮肤中角质化包膜电子密度的连续变化这一恒定特征在EH中常常缺失。这些结果提示EH中角质化包膜的组装过程发生了改变。