Azzarone B, Macieira-Coelho A
Exp Cell Res. 1984 Nov;155(1):299-304. doi: 10.1016/0014-4827(84)90794-8.
Giant axonal neuropathy skin fibroblasts, which are characterized by a selective and partial disorganization of vimentin filaments [1] exhibited, when compared with normal skin fibroblasts, less fibrin clot retractile (FCR) activity and spreading within the fibrin clot both during active growth and resting stage. Skin fibroblasts derived from patients affected with adenomatosis of the colon and rectum, which display a disorganized actin network [2], exhibited reduced FCR activity and spreading within the fibrin clot only during resting stage. FCR inhibition was also obtained by treating the cells with colcemid, cytochalasin B (CB) and dihydrocytochalasin B. The data suggest that FCR activity is under the control of different cytoskeletal structures. For the first time, a direct involvement of intermediate-sized filaments could be demonstrated in the interaction between fibroblasts and an organic substratum.
巨大轴索性神经病皮肤成纤维细胞的特征是波形蛋白丝存在选择性和部分紊乱[1]，与正常皮肤成纤维细胞相比，在活跃生长和静止期，其纤维蛋白凝块收缩（FCR）活性较低，且在纤维蛋白凝块内的铺展能力较弱。来自结肠和直肠腺瘤病患者的皮肤成纤维细胞表现出肌动蛋白网络紊乱[2]，仅在静止期其FCR活性降低且在纤维蛋白凝块内的铺展能力减弱。用秋水仙酰胺、细胞松弛素B（CB）和二氢细胞松弛素B处理细胞也可抑制FCR。数据表明，FCR活性受不同细胞骨架结构的控制。首次证明了中等大小的细丝可直接参与成纤维细胞与有机基质之间的相互作用。
