Shabana A H, Oboeuf M, Forest N
Laboratoire de Biologie-Odontologie, Institut Biomédical des Cordeliers, France.
Tissue Cell. 1994 Feb;26(1):43-55. doi: 10.1016/0040-8166(94)90082-5.
The present paper describes disturbances in the organization of tonofilaments and desmosomes of rat lingual and epidermal keratinocytes after treatment of the cells with acrylamide in culture. This treatment induced changes in cell shape, reduction of intercellular adhesion and a perinuclear accumulation of cytoplasmic organelles. Using specific antibodies for cytokeratins, the filaments were disorganized particularly in the perinuclear region. In untreated cells, keratin filament labelling was very weak or absent above and below the nucleus thus leaving a black nuclear space in fluorescine microscopy. Following acrylamide treatment, the keratin filament labelling covered the nuclear space which indicated the accumulation of these filaments all around the nucleus. Furthermore, the desmosomal junctions were often associated with thick keratin bundles. Antibodies for desmoplakins revealed a reduction in intercellular labelling and stronger cytoplasmic labelling. Ultrastructurally, well-developed long tonofilaments were found to associate with large desmosomal junctions. Furthermore, small-sized desmosomal structures were identified within the cytoplasm. Morphologically, these were identical to cell surface desmosomes and were almost always associated with well-developed tonofilaments. The effect of acrylamide on the protein kinase A activity might be implicated in the disturbances of the desmosome-intermediate filament complex and in the initiation of contractile forces necessary for perinuclear accumulation of intermediate filaments and for the formation of intact cytoplasmic desmosomes. The acrylamide-induced intermediate filament and desmosomal changes may provide valuable information on the mechanism of intact cytoplasmic desmosome formation in several skin diseases and in squamous cell carcinoma.
本文描述了在培养条件下用丙烯酰胺处理大鼠舌和表皮角质形成细胞后，张力丝和桥粒组织的紊乱情况。这种处理导致细胞形态改变、细胞间黏附力降低以及细胞质细胞器在核周积聚。使用细胞角蛋白特异性抗体，发现张力丝尤其在核周区域紊乱。在未处理的细胞中，在细胞核上方和下方，角蛋白丝标记非常弱或不存在，因此在荧光显微镜下留下黑色的核间隙。丙烯酰胺处理后，角蛋白丝标记覆盖了核间隙，这表明这些丝在细胞核周围积聚。此外，桥粒连接通常与粗大的角蛋白束相关。桥粒斑蛋白抗体显示细胞间标记减少，细胞质标记增强。超微结构上，发现发育良好的长张力丝与大型桥粒连接相关。此外，在细胞质内还鉴定出小型桥粒结构。从形态学上看，这些与细胞表面桥粒相同，并且几乎总是与发育良好的张力丝相关。丙烯酰胺对蛋白激酶A活性的影响可能与桥粒-中间丝复合体的紊乱以及中间丝在核周积聚和完整细胞质桥粒形成所需收缩力的启动有关。丙烯酰胺诱导的中间丝和桥粒变化可能为几种皮肤病和鳞状细胞癌中完整细胞质桥粒形成的机制提供有价值的信息。
