Suppr超能文献

离子和细胞外蛋白在白细胞运动和膜皱褶形成中的作用。

Role of ions and extracellular protein in leukocyte motility and membrane ruffling.

作者信息

Mukherjee C, Lynn W S

出版信息

Am J Pathol. 1978 Nov;93(2):369-81.

Abstract

Ruffling and motility, either directed or random, of polymorphonuclear leukocytes (PMNL) were shown to require a monovalent cation (MC). Na+ and Li+ are most effective. These MC-dependent activities are modulated by nonspecific proteins and peptides and are inhibited by cytochalasin B and by alkylating agents such as TPCK (L-[tosylamide-2-phenyl]ethylchloromethyl ketone) but not by ouabain or colchicine. The modulation by protein, but not the inhibition by TPCK or cytochalasin, is competitively inhibited by hydrophobic chemotactic peptides such as f.met-phe and f.phe-met. These hydrophobic peptides, which activate MC influx, promote motility at low concentrations of Na+ (0.1 mM); however, at higher concentrations of Na+ (1.0 mM) the same concentrations of peptides inhibit motility. This inhibition is the result of excessive Na+ and water influx with resultant cellular swelling. The chemotactic peptides, when present as a concentration gradient, function in chemotaxis by competing with the protein at the leading edge of the cell, with resultant local ion influx and swelling. Hydrolysis of the peptide is not required since protease inhibitors have no specific effect on peptide directed migration, although they do inhibit migration. Since local influx of MC and H2O with resultant hydrolysis of ATP is absolutely required for all motility in these cells, it is likely that local swelling and depolymerization of the actin cytoskeletal system are the primary reversible events in PMNL motility. This local swelling or ruffling apparently results in the pushing of cellular contents into the relaxed swollen submembrane areas of the cell by continued contraction of unswollen areas of the cell.

摘要

多形核白细胞(PMNL)的边缘波动和运动性,无论是定向的还是随机的,都显示需要一价阳离子(MC)。Na+和Li+最为有效。这些依赖于MC的活动受到非特异性蛋白质和肽的调节,并被细胞松弛素B和烷基化剂如TPCK(L-[甲苯磺酰胺-2-苯基]乙基氯甲基酮)抑制,但不受哇巴因或秋水仙碱抑制。蛋白质的调节作用,但不是TPCK或细胞松弛素的抑制作用,被疏水性趋化肽如f.met-phe和f.phe-met竞争性抑制。这些疏水性肽激活MC内流,在低浓度Na+(0.1 mM)时促进运动性;然而,在较高浓度的Na+(1.0 mM)时,相同浓度的肽抑制运动性。这种抑制是由于过量的Na+和水内流导致细胞肿胀的结果。趋化肽以浓度梯度存在时,通过与细胞前缘的蛋白质竞争发挥趋化作用,导致局部离子内流和肿胀。肽的水解不是必需的,因为蛋白酶抑制剂对肽介导的迁移没有特异性影响,尽管它们确实抑制迁移。由于MC和H2O的局部内流以及由此导致的ATP水解对于这些细胞的所有运动性绝对必要,因此肌动蛋白细胞骨架系统的局部肿胀和解聚可能是PMNL运动性中的主要可逆事件。这种局部肿胀或边缘波动显然导致细胞内容物通过细胞未肿胀区域的持续收缩被推入细胞松弛的肿胀亚膜区域。

相似文献

引用本文的文献

本文引用的文献

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