Suppr超能文献

层粘连蛋白和细胞骨架因子对NG108-15细胞神经突形成的影响。

Effect of laminin and cytoskeletal agents on neurite formation by NG108-15 cells.

作者信息

Luckenbill-Edds L, Kleinman H K

机构信息

Laboratory of Developmental Biology and Anomalies, National Institute of Dental Research, Bethesda, Maryland.

出版信息

J Neurosci Res. 1988 Feb;19(2):219-29. doi: 10.1002/jnr.490190207.

Abstract

Laminin promotes attachment and process formation in the neuroblastoma X glioma hybrid cell line NG108-15. As cells attached to laminin, they flattened and remained dispersed rather than associated in clumps. Process formation was observed within 1 hr after exposure to laminin and was dose dependent. Cycloheximide, an inhibitor of protein synthesis, did not block laminin-mediated attachment and neurite formation. Addition of drugs that depolymerize the cytoskeleton led to different behaviors for cells grown on plastic compared with those in the presence of laminin. Cells on plastic treated with either vinblastine or cytochalasin neither flattened nor grew processes. Cells plus laminin and vinblastine retracted processes, but remained flat, suggesting that laminin-induced processes can be destabilized by disrupting microtubules. Cells sequentially treated with laminin and cytochalasin produced processes that were thin and highly branched. Cells in high concentrations of cytochalasin on a laminin substrate formed aberrant processes even when their soma did not flatten. Since laminin counteracted the effect of cytochalasin on process outgrowth but did not alter the effect of cytochalasin on flattening of the cell body, different mechanisms mediated by microfilaments may be involved in cell flattening and in process formation.

摘要

层粘连蛋白可促进神经母细胞瘤X胶质瘤杂交细胞系NG108 - 15的附着和突起形成。当细胞附着于层粘连蛋白时,它们会变平并保持分散状态,而不是聚集成团。在接触层粘连蛋白后1小时内可观察到突起形成,且呈剂量依赖性。蛋白质合成抑制剂环己酰亚胺并不阻断层粘连蛋白介导的附着和神经突形成。与在层粘连蛋白存在下生长的细胞相比,添加使细胞骨架解聚的药物会导致在塑料上生长的细胞出现不同行为。用长春花碱或细胞松弛素处理过的塑料上的细胞既不变平也不生长突起。添加层粘连蛋白和长春花碱的细胞会使突起缩回,但仍保持扁平,这表明层粘连蛋白诱导的突起可因破坏微管而变得不稳定。先后用层粘连蛋白和细胞松弛素处理的细胞会产生细且高度分支的突起。即使细胞体没有变平,在层粘连蛋白底物上处于高浓度细胞松弛素中的细胞也会形成异常突起。由于层粘连蛋白抵消了细胞松弛素对突起生长的影响,但并未改变细胞松弛素对细胞体变平的影响,因此微丝介导的不同机制可能参与了细胞变平和突起形成过程。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验