Amar L S, Oboeuf M, Martin N, Forest N
Laboratoire de Biologie-Odontologie, Université Paris, France.
Cell Adhes Commun. 1998 Jan;5(1):1-12. doi: 10.3109/15419069809005594.
In the present study, we addressed the possible relevance of protein kinase C (PKC) in the regulation of intracytoplasmic desmosome assembly. Treatment of cultured rat lingual and epidermal keratinocytes with a potent and highly selective PKC inhibitor (GF109203X) induced an increase in granular labelling for major desmosomal proteins, desmoplakins, desmoglein and plakoglobin, both intracellularly and at the cell surface. This was associated with the formation of ultrastructurally recognizable desmosomes deep in the cytoplasm and increase in intercellular desmosome number. In contrast, PKC activation upon short exposure to 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in altered cell morphology, loss of intercellular contact and accumulation of desmosomal proteins in the juxtanuclear zone. On the other hand, PKC depletion by long term TPA treatment re-established cell-cell contact, where desmosomal markers were exclusively redistributed. Taken together, these results suggest that inhibition of PKC is required for intracytoplasmic as well as intercellular desmosome assembly, whereas its activation may regulate disassembly process.
在本研究中，我们探讨了蛋白激酶C（PKC）在调节细胞质内桥粒组装中的潜在相关性。用一种强效且高度选择性的PKC抑制剂（GF109203X）处理培养的大鼠舌和表皮角质形成细胞，导致主要桥粒蛋白、桥粒斑蛋白、桥粒芯糖蛋白和桥粒胶蛋白在细胞内和细胞表面的颗粒状标记增加。这与细胞质深处超微结构可识别的桥粒形成以及细胞间桥粒数量增加有关。相反，短时间暴露于12 - O - 十四酰佛波醇13 - 乙酸酯（TPA）后PKC激活导致细胞形态改变、细胞间接触丧失以及桥粒蛋白在核周区积累。另一方面，长期TPA处理导致PKC耗竭后重新建立了细胞 - 细胞接触，此时桥粒标记物仅重新分布。综上所述，这些结果表明，细胞质内以及细胞间桥粒组装需要抑制PKC，而其激活可能调节拆解过程。
