Paller A S, Arnsmeier S L, Fisher G J, Yu Q C
Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois 60614.
Exp Cell Res. 1995 Mar;217(1):118-24. doi: 10.1006/excr.1995.1070.
The altered patterns of expression of gangliosides during density-dependent growth inhibition, oncogenic transformation, and embryogenesis suggest that gangliosides, sialylated membrane glycolipids, may affect cellular proliferation and differentiation. Gangliosides of the "b" pathway of ganglioside synthesis, including GM3, GD3, and GD1b, inhibit the proliferation of cultured keratinocytes without increasing differentiation. We have examined the effect on keratinocyte proliferation and differentiation of supplemental ganglioside GT1b, a more highly sialylated ganglioside of the "b" synthetic pathway that is also present in cultured keratinocytes. In contrast to the lack of effect on differentiation of these other gangliosides, we noted significant induction of keratinocyte differentiation by GT1b, as evidenced by early desmosome formation, and increased cornified envelope formation and expression of involucrin and of the differentiation-specific keratin K1. The addition of GT1b did not cause a shift in intracellular free calcium or alter protein kinase C activity. Alterations in the membrane concentration of ganglioside GT1b, a minor ganglioside component of the keratinocyte membrane, may participate in regulating keratinocyte differentiation.
神经节苷脂在密度依赖性生长抑制、致癌转化和胚胎发生过程中表达模式的改变表明，神经节苷脂这种唾液酸化的膜糖脂可能会影响细胞增殖和分化。神经节苷脂合成“b”途径的神经节苷脂，包括GM3、GD3和GD1b，可抑制培养的角质形成细胞的增殖，而不会增加其分化。我们研究了补充神经节苷脂GT1b对角质形成细胞增殖和分化的影响，GT1b是“b”合成途径中一种唾液酸化程度更高的神经节苷脂，也存在于培养的角质形成细胞中。与其他神经节苷脂对分化缺乏影响相反，我们注意到GT1b可显著诱导角质形成细胞分化，早期桥粒形成、角质化包膜形成增加以及内披蛋白和分化特异性角蛋白K1的表达增加都证明了这一点。添加GT1b不会导致细胞内游离钙的变化，也不会改变蛋白激酶C的活性。神经节苷脂GT1b是角质形成细胞膜中的一种次要神经节苷脂成分，其膜浓度的改变可能参与调节角质形成细胞的分化。
