Beta-interferon-induced time-dependent changes in the plasma membrane lipid bilayer of cultured cells.
Beta-interferon-induced time-dependent changes in the plasma membrane lipid bilayer of cultured cells.
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DOI：
10.1089/jir.1981.1.613
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
L. Pfeffer;F. Landsberger;I. Tamm
中科院分区：
文献类型：
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作者：
L. Pfeffer;F. Landsberger;I. Tamm
利用自旋标记电子自旋共振技术在培养细胞中研究了干扰素诱导的质膜脂双分子层的时间依赖性结构变化。人β - 1干扰素（640 u/ml）对悬浮培养的人HeLa-S3细胞处理30min后，质膜脂双分子层的硬度增加（Landsberger， Pfeffer和Tamm，准备中）。干扰素处理细胞的质膜硬度在3 ~ 5小时内恢复到对照细胞的水平，但在开始治疗后24小时，质膜硬度再次增加，并保持至少2天。小鼠β干扰素在同源小鼠L-929细胞中引起早期（Landsberger， Pfeffer和Tamm， in preparation）和晚期膜刚性增加，但在异种HeLa-S3细胞中没有引起。因此，干扰素诱导的膜结构扰动是物种特异性的。膜刚度的后期增加可能与早期增加有不同的潜在机制。虽然早期和短暂的变化可能与信号的产生和传递有关，但后期和持续的变化可能是表型和干扰素处理细胞的一个方面，可能反映了质膜-细胞骨架复合物的变化。
The time-dependent interferon-induced structural changes in the plasma membrane lipid bilayer have been investigated in cultured cells using spin label electron spin resonance techniques. Treatment of human HeLa-S3 cells in suspension culture with human beta 1 interferon (640 u/ml) for as short a time as 30 min causes an increase in the rigidity of the plasma membrane lipid bilayer (Landsberger, Pfeffer and Tamm, in preparation). The plasma membrane rigidity of interferon-treated cells returns to the level of control cells within 3 to 5 hr, but by 24 hr after beginning of treatment, the rigidity of the plasma membrane is increased again and remains so for at least 2 days. Mouse beta interferon causes both an early (Landsberger, Pfeffer and Tamm, in preparation) and a late increase in membrane rigidity in homologous mouse L-929 cells, but not in heterologous HeLa-S3 cells. Thus, the interferon-induced perturbation of membrane structure is species specific. The late increase in membrane rigidity may have a different underlying mechanism from that of the early increase. While the early and transient change probably is related to signal generation and transmission, the later and persistent change may be an aspect of the phenotype and interferon-treated cells and may reflect changes in the plasma membrane-cytoskeletal complex.