Internalization of cationized ferritin into the Golgi complex of cultured mouse peritoneal macrophages. Effects of colchicine and cytochalasin B.

Internalization of cationized ferritin into the Golgi complex of cultured mouse peritoneal macrophages. Effects of colchicine and cytochalasin B.
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阳离子铁蛋白内化到培养的小鼠腹膜巨噬细胞的高尔基复合体中。

DOI:
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发表时间:
1980
影响因子:
6.6
通讯作者:
J. Thyberg
J. Thyberg
中科院分区:
生物学3区
文献类型:
--
作者:
J. Thyberg

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体外培养小鼠腹膜巨噬细胞,暴露于外源性示踪剂,透射电镜观察。天然的阴离子铁蛋白和辣根过氧化物酶不与细胞表面结合,在被吸收进入细胞后只存在于内吞囊泡和溶酶体中。阳离子化铁蛋白(CF)与质膜结合,然后迅速内化。在细胞内,CF首先到达溶酶体,但随后也转移到并通过高尔基复合体。这些结果初步提示,在巨噬细胞内,部分内吞囊泡的内容物和膜可能遵循不同的途径。内容物被排空到溶酶体中,从溶酶体中进入的膜的一部分随后可以分离并移动到高尔基复合体中进行再利用。另外,在用乳胶珠和CF进行的双标记实验中获得了支持这一观点的间接证据。因此,正如预期的那样,关于含有乳胶的吞噬溶酶体的持久性,暴露于两种示踪物的细胞中CF向高尔基复合体的转移比单独暴露于CF的细胞要小得多。用秋水秋碱预处理巨噬细胞去除所有细胞质微管,导致高尔基复合物的特征性紊乱。然而,处理不干扰CF与质膜的结合,但明显抑制其摄取和运输到高尔基体复合体。相反,lumicolchinine和cytochalasin B不影响CF的摄取和细胞内目的地。这些结果证实了先前关于细胞质微管在胞吞作用中的作用的观点。他们进一步指出,微管的缺失会影响细胞内结合到细胞表面的分子的处理。
Mouse peritoneal macrophages were cultured in vitro, exposed to exogenous tracers, and examined by transmission electron microscopy. Native, anionic ferritin and horseradish peroxidase did not bind to the cell surface and were exclusively found in endocytic vesicles and lysosomes after uptake into the cells. Cationized ferritin (CF) bound to the plasma membrane and was then rapidly internalized. Intracellularly, CF first reached the lysosomes, but was later also transferred to and passed through the Golgi complex. These findings tentatively suggest that content and membrane of endocytic vesicles partly may follow different routes within macrophages. The content is emptied into lysosomes, from which part of the incoming membrane subsequently can be detached and moved over to the Golgi complex for reutilization. Additional, indirect evidence in support of this idea was obtained in double-labeling experiments with latex beads and CF. Thus, as expected with regard to the persistent nature of the latex-containing phagolysosomes, the transfer of CF to the Golgi complex was of a much smaller magnitude in cells exposed to both tracers than in cells exposed to CF alone. Pretreatment of the macrophages with colchicine removed all cytoplasmic microtubules and led to a characteristic disorganization of the Golgi complex. The treatment did not interfere with the binding of CF to the plasma membrane, however, but distinctly inhibited its uptake and transport to the Golgi complex. Contrarily, lumicolchicine and cytochalasin B did not affect the uptake and intracellular destination of CF. These results confirm previous notions concerning a role of cytoplasmic microtubules in endocytosis. They further indicate that absence of microtubules affects the intracellular handling of molecules binding to the cell surface.