胆固醇氧化酶和羟甲基戊二酰辅酶A还原酶抑制剂甲维苷干扰培养血管平滑肌细胞的内吞运输。

J Thyberg
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引用次数: 0

摘要

胆固醇是细胞膜的一种成分,尤其丰富于小泡(50-80纳米的质膜瓶状内陷)。小泡在血管内皮细胞和平滑肌细胞中数量众多,并参与多种功能,包括信号转导、脂质转运和大分子摄取。在无血清原代培养物中,研究了在纤维连接蛋白底物上生长的大鼠主动脉平滑肌细胞中,胆固醇氧化酶(一种氧化活细胞小窝中胆固醇的酶)和甲维苷(一种胆固醇合成抑制剂)对外源性标志物精细结构和内化的影响。胆固醇氧化酶引起内吞室的增大,内核体和含示踪分子的溶酶体增大。与此同时,小泡的数量减少了约五分之一。此外,高尔基复合体的形态发生了变化,肿胀的池被空洞的液泡包围。甲维林可抑制细胞从分化或收缩型向去分化或合成型的转变。此外,发现收缩细胞不仅将辣根过氧化物酶(HRP)摄取到核内体和溶酶体中,而且还摄取到高尔基池中,特别是在堆栈的凸/顺侧和内质网中。在暴露于霍乱毒素B亚基(CTB)-HRP偶联物的收缩细胞中发现了类似的途径,这是一种与神经节苷脂GM1结合的配体,至少部分通过小泡被摄入。melvinolin并没有阻止cvb - hrp向高尔基复合物的转运,但在这种情况下,共轭物集中在池堆的凹/反侧。然而,对小泡的数量没有明显的影响。观察结果表明胆固醇和小泡在平滑肌细胞内吞运输的控制中的重要作用。这种功能在细胞处于分化状态时表现得最为显著。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cholesterol oxidase and the hydroxymethylglutaryl coenzyme A reductase inhibitor mevinolin perturb endocytic trafficking in cultured vascular smooth muscle cells.

Cholesterol is a component of cellular membranes and especially abundant in caveolae (50-80 nm flask-shaped invaginations of the plasma membrane). Caveolae are highly numerous in vascular endothelial and smooth muscle cells and have been implicated in a variety of functions, including signal transduction, lipid transport and uptake of macromolecules. Here, the effects of cholesterol oxidase (an enzyme that oxidizes cholesterol in caveolae of living cells) and mevinolin (an inhibitor of cholesterol synthesis) on fine structure and internalization of exogenous markers were studied in rat aortic smooth muscle cells grown on a substrate of fibronectin in serum-free primary cultures. Cholesterol oxidase caused a growth in size of the endocytic compartment with accumulation of enlarged endosomes and lysosomes containing tracer molecules. In parallel, the number of caveolae was reduced by about one fifth. Moreover, the morphology of the Golgi complex was altered with swollen cisternae surrounded by empty-looking vacuoles. Mevinolin suppressed transition of the cells from a differentiated or contractile to a dedifferentiated or synthetic phenotype. In addition, contractile cells were found to ingest horseradish peroxidase (HRP) not only into endosomes and lysosomes but also into Golgi cisternae, especially on the convex/cis side of the stacks, and the endoplasmic reticulum. A similar pathway was noted in contractile cells exposed to cholera toxin B subunit (CTB)-HRP conjugates, a ligand that binds to ganglioside GM1 and at least in part is ingested via caveolae. Mevinolin did not prevent the transport of CTB-HRP to the Golgi complex, but the conjugates were in this case concentrated to the concave/trans side of the cisternal stacks. However, no clear effect on the number of caveolae was noted. The observations indicate an important role of cholesterol and caveolae in the control of endocytic traffic in smooth muscle cells. This function appears most significant when the cells are in a differentiated state.

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