Clementi F, Sher E, Erroi A
Eur J Cell Biol. 1983 Jan;29(2):274-80.
The continuous muscle cell line BC3-H1, which expresses nicotinic Acetylcholine receptors (AChR) at the cell surface, was used to study the effect of lysosomotropic drugs on AChR degradation both in the normal condition and after stimulation induced by treatment with anti-AChR antibodies. We found that ammonium chloride, methylamine, and bacitracin decreased AChR degradation both in normal and stimulated cells but did not prevent AChR internalization from the cell surface. In addition NH4Cl increased size and number of lysosomes in treated cells, while methylamine and bacitracin did not. These latter drugs increased the Golgi area and the vesicular complement of the Golgi apparatus. It is proposed that the drugs used decrease AChR degradation by interfering either with lysosome function, or with the fusion of endosomes with lysosomes. The data also suggest that AChR degradation induced by anti-AChR antibodies is carried out by a mechanism similar to that accounting for AChR degradation in control cells.
连续肌肉细胞系BC3-H1在细胞表面表达烟碱型乙酰胆碱受体（AChR），用于研究溶酶体促渗药物在正常条件下以及在用抗AChR抗体处理诱导刺激后对AChR降解的影响。我们发现氯化铵、甲胺和杆菌肽在正常细胞和受刺激细胞中均降低了AChR的降解，但并未阻止AChR从细胞表面内化。此外，NH4Cl增加了处理细胞中溶酶体的大小和数量，而甲胺和杆菌肽则没有。后两种药物增加了高尔基体区域和高尔基体的囊泡成分。有人提出，所使用的药物通过干扰溶酶体功能或内体与溶酶体的融合来减少AChR的降解。数据还表明，抗AChR抗体诱导的AChR降解是通过一种类似于对照细胞中AChR降解机制进行的。
