Collins V P
Cytobiologie. 1978 Dec;18(2):327-38.
Human glia cells become blocked in G1 if starved of serum. The characteristics of the GI blocked state are flattening on the substrate, and absence of cell translocation, ruffling and macropinocytosis. Re-entry into the cell cycle, as a result of growth factor stimulation, is accompained and even preceded by the return of this cellular locomotion. We have studied the fine structure of intact human glia cells and ultrathin sections of these cells when proliferating normally in vitro, when starved of serum and during their return to the cell cycle following stimulation with mEGF (mouse epidermal growth factor). Particular attention was paid to morphologically definable components of the cellular musculoskeletal system. Proliferating interphase glia generally had a leading lamella containing few organelles and oriented bundles of 7 nm microfilaments with structureless lamellipodia at their tips, which often formed ruffles. The perinuclear area was thick and contained many cell organelles, including mitochondria and secondary lysosomes. Glia starved of serum were thinly spread; their peripheral cytoplasm was filled with a diffuse mat of microfilaments, they had no structureless lamellipodia and their perinuclear areas, although thinner, contained cell organelles in equal amounts and of similar type of those found in proliferating cells. On EGF stimulation, after approximately 2 hours the perinuclear area of the cells thickened, and structureless lamellipodia subsequently appeared at the tips of the leading lamellae, forming ruffles. The cells finally began to translocate, the process being accompained by the reorientation and packing of the microfilaments into bundles. As the kinetics of EGF binding and break down by glia cells are similar to those described for fibroblasts, the findings do not support the concept of EGF receptor interactions inducing ultrastructurally demonstrable microfilament or other musculoskeletal structural changes in the cell. They do, however, define the differing cellular morphologies of motile and immobile structures.
如果血清饥饿，人类神经胶质细胞会在G1期受阻。G1期受阻状态的特征是在底物上变平，且不存在细胞易位、褶皱和巨胞饮作用。由于生长因子刺激而重新进入细胞周期，伴随着甚至先于这种细胞运动的恢复。我们研究了完整人类神经胶质细胞的精细结构以及这些细胞在体外正常增殖、血清饥饿时以及用小鼠表皮生长因子（mEGF）刺激后恢复细胞周期期间的超薄切片。特别关注了细胞肌肉骨骼系统中形态上可定义的成分。增殖的间期神经胶质细胞通常有一个含较少细胞器的前缘薄片，其顶端有7纳米微丝的定向束和无结构的片状伪足，片状伪足常形成褶皱。核周区域较厚，含有许多细胞器，包括线粒体和次级溶酶体。血清饥饿的神经胶质细胞铺展得很薄；它们的外周细胞质充满了微丝的弥散网，没有无结构的片状伪足，其核周区域虽然较薄，但含有与增殖细胞中数量相等且类型相似的细胞器。在EGF刺激后，大约2小时后细胞的核周区域变厚，随后在领先薄片的顶端出现无结构的片状伪足，形成褶皱。细胞最终开始易位，这个过程伴随着微丝重新定向并聚集成束。由于神经胶质细胞结合和分解EGF的动力学与成纤维细胞所描述的相似，这些发现不支持EGF受体相互作用诱导细胞中超微结构上可证明的微丝或其他肌肉骨骼结构变化的概念。然而，它们确实定义了活动和不活动结构的不同细胞形态。
