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小鼠红白血病细胞的相互接触会激活去极化阳离子通道,而与细胞外基质接触则会激活超极化的钙依赖性钾通道。

Mutual contact of murine erythroleukemia cells activates depolarizing cation channels, whereas contact with extracellular substrata activates hyperpolarizing Ca2+-dependent K+ channels.

作者信息

Arcangeli A, Riccarda Del Bene M, Poli R, Ricupero L, Olivotto M

机构信息

Institute of General Pathology, Medical Faculty, University of Florence, Firenze, Italy.

出版信息

J Cell Physiol. 1989 Apr;139(1):1-8. doi: 10.1002/jcp.1041390102.

DOI:10.1002/jcp.1041390102
PMID:2468677
Abstract

This study deals with the modulation of the plasma membrane potential (delta psi p) of murine erythroleukemia (MEL) cells by cell-substratum or cell-cell contact. delta psi p was determined by measuring the distribution of tetraphenylphosphonium (TPP+) across the plasma membrane; it appeared strongly, and inversely, influenced by the two types of cell contacts. Contact with the culture surface produced a delta psi p hyperpolarization directly proportional to average distance among the ideal centers of the cells on this surface (d) within the range 10-80 microns. A detailed mathematical analysis of the function delta psi p = f(d) is presented, as well as experiments involving the use of ionophores (valinomycin and A23187) and the conditioning of the culture surface. We concluded that the d-dependent hyperpolarization (dDH) was the result of a complex interplay between the activating properties of substratum on Ca2+-dependent K+ channels (KCa) and some substratum-adherent factors that are shed by MEL cells and antagonize KCa activation (substratum-attached cellular factors = SACF). By contrast, contact of the cells with each other, obtained by incubating MEL cells at d smaller than the average cell diameter (phi = 10 microns), produced a marked delta psi p depolarization. This intercellular contact-dependent depolarization (ICDD) was unaffected by valinomycin; it was abolished by substituting Na+ in the external medium with a nondiffusible cation (choline), which shows that ICDD was sustained by Na+ influxes, probably mediated by stretch-activated (s.a.) cation channels.

摘要

本研究探讨了细胞与基质或细胞与细胞接触对小鼠红白血病(MEL)细胞质膜电位(δψp)的调节作用。通过测量四苯基鏻(TPP +)在质膜上的分布来确定δψp;结果表明,这两种细胞接触对其有强烈且相反的影响。与培养表面接触会使δψp超极化,在10 - 80微米范围内,这种超极化与该表面上细胞理想中心之间的平均距离(d)成正比。本文给出了δψp = f(d)函数的详细数学分析,以及涉及使用离子载体(缬氨霉素和A23187)和培养表面预处理的实验。我们得出结论,d依赖性超极化(dDH)是基质对钙依赖性钾通道(KCa)的激活特性与MEL细胞释放的一些拮抗KCa激活的基质黏附因子(基质附着细胞因子 = SACF)之间复杂相互作用的结果。相比之下,通过将MEL细胞在小于平均细胞直径(φ = 10微米)的d下孵育获得的细胞间相互接触,会产生明显的δψp去极化。这种细胞间接触依赖性去极化(ICDD)不受缬氨霉素影响;用非扩散性阳离子(胆碱)替代外部培养基中的Na +可消除这种去极化,这表明ICDD是由Na +内流维持的,可能是由牵张激活(s.a.)阳离子通道介导的。

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