Enhancement of keratin synthesis induced by lipokeratinogenoside, N-(O-linoleoyl)-omega-hydroxy fatty acyl sphingosyl glucose, in association with alteration of the intracellular Ca(2+)-content and protein kinase in cultured keratinocytes (FRSK).
Enhancement of keratin synthesis induced by lipokeratinogenoside, N-(O-linoleoyl)-omega-hydroxy fatty acyl sphingosyl glucose, in association with alteration of the intracellular Ca(2+)-content and protein kinase in cultured keratinocytes (FRSK).
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脂角蛋白原苷、N-(O-亚油酰基)-omega-羟基脂肪酰基鞘氨醇葡萄糖诱导的角蛋白合成增强，与培养的角质形成细胞 (FRSK) 中细胞内 Ca(2) 含量和蛋白激酶的改变有关。
DOI：
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发表时间：
1991
期刊：
影响因子：
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通讯作者：
Y. Nagai
中科院分区：
文献类型：
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作者：
Y. Uchida;T. Ogawa;M. Iwamori;Y. Nagai
脂角蛋白苷[N-（o -亚油基）-omega-羟基脂肪酸酰基鞘脂-葡萄糖]是一种表皮苷，是哺乳动物皮肤表皮特有的鞘脂糖。在培养的大鼠角质形成细胞（FRSK）中添加脂角蛋白基因苷后，培养48和144 h后，细胞中角蛋白的数量增加，是未添加脂角蛋白基因苷的1.4 ~ 1.8倍，并且在添加脂角蛋白基因苷的细胞中，角质包膜的数量也显著增加。抗角蛋白抗体免疫组化染色显示，与对照细胞相比，脂角蛋白苷培养的细胞被密集的角蛋白覆盖。在TPA的存在下，角蛋白和角化包膜的合成也得到了同样的增强，这已经被证明可以提高细胞内Ca（2+）含量，并在跨膜信号传导的初始阶段将细胞质蛋白激酶C转移到质膜上。同样，脂角化蛋白皂苷显示出与TPA相同程度的增加细胞内Ca（2+）含量的能力，并将蛋白激酶C转移到膜部分。然而，随着亚油酸部分被温和碱去除，脂角化蛋白皂苷的上述活性降低，但单独亚油酸不表现出任何活性，表明脂角化蛋白皂苷分子本身需要表达活性。
Lipokeratinogenoside [N-(O-linoleoyl)-omega-hydroxy fatty acyl sphingosyl beta-glucose] is one of the epidermosides which were found to be glycosphingolipids characteristic of the epidermis of mammalian skin. On the addition of lipokeratinogenoside to cultured rat keratinocytes (FRSK), the amount of keratin in the cells increased, 48 and 144 h after cultivation, to 1.4 to 1.8 times higher than that without the addition of lipokeratinogenoside, and the number of cornified envelopes also significantly increased on cultivation of the cells with lipokeratinogenoside. Immunohistochemical staining with anti-keratin antibody revealed that the cells cultivated with lipokeratinogenoside were densely covered with keratin in distinct contrast to the control cells. The same enhanced syntheses of keratin and cornified envelopes were observed on cultivation in the presence of TPA, which has been shown to elevate the intracellular Ca(2+)-content and to translocate cytoplasmic protein kinase C to the plasma membrane in the initial stage of transmembrane signalling. Similarly, lipokeratinogenoside showed the ability to increase the intracellular Ca(2+)-content to the same extent as TPA did and to translocate protein kinase C to the membrane fraction. However, the above activities of lipokeratinogenoside decreased with removal of the linoleic acid moiety from lipokeratinogenoside with mild alkali, but linoleic acid alone did not show any activities, indicating that the lipokeratinogenoside molecule itself is required for expression of the activities.