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首页> 外文期刊>Journal of Cellular Physiology >Pantethine Alters Lipid Composition and Cholesterol Content of Membrane Rafts, With Down-Regulation of CXCL12-Induced T Cell Migration
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Pantethine Alters Lipid Composition and Cholesterol Content of Membrane Rafts, With Down-Regulation of CXCL12-Induced T Cell Migration

机译：Pantethine改变脂质成分和的膜筏、胆固醇含量下调CXCL12-Induced T细胞迁移

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摘要

Pantethine, a natural low-molecular-weight thiol, shows a broad activity in a large range of essential cellular pathways. It has been long known as a hypolipidemic and hypocholesterolemic agent. We have recently shown that it exerts a neuroprotective action in mouse models of cerebral malaria and Parkinson's disease through multiple mechanisms. In the present study, we looked at its effects on membrane lipid rafts that serve as platforms for molecules engaged in cell activity, therefore providing a target against inappropriate cell response leading to a chronic inflammation. We found that pantethine-treated cells showed a significant change in raft fatty acid composition and cholesterol content, with ultimate downregulation of cell adhesion, CXCL12-driven chemotaxis, and transendothelial migration of various T cell types, including human Jurkat cell line and circulating effector T cells. The mechanisms involved include the alteration of the following: (i) CXCL12 binding to its target cells; (ii) membrane dynamics of CXCR4 and CXCR7, the two CXCL12 receptors; and (iii) cell redox status, a crucial determinant in the regulation of the chemokine system. In addition, we considered the linker for activation of T cells molecule to show that pantethine effects were associated with the displacement from the rafts of the acylated signaling molecules which had their palmitoylation level reduced. In conclusion, the results presented here, together with previously published findings, indicate that due to its pleiotropic action, pantethine can downregulate the multifaceted process leading to pathogenic T cell activation and migration.
机译：Pantethine,自然低分子量硫醇显示了一个广泛的在一个大范围的活动重要的细胞通路。称为降血脂药和hypocholesterolemic代理。小鼠模型的神经保护作用脑型疟疾和帕金森病多种机制。看着它对膜脂质筏的影响作为分子参与的平台细胞活性,因此提供一个目标对导致不适当的细胞反应慢性炎症。pantethine-treated细胞表现出显著筏脂肪酸组成和变化以上。差别胆固醇含量,最终对这些细胞粘附,CXCL12-driven趋化作用,transendothelial各种T细胞的迁移类型,包括人类Jurkat细胞系循环效应T细胞。涉及的变更包括以下几点:(我)CXCL12绑定到其靶细胞;趋化因子受体CXCR4和CXCR7膜动力学、两个CXCL12受体;监管的重要因素趋化因子系统。链接器激活T细胞的分子pantethine效应相关位移的木筏acylated有他们的信号分子棕榈酰化水平降低。这里给出的结果,加上之前公布调查结果,表明由于它多效性的行动,pantethine可以表达下调多方面的过程导致致病性T细胞活化和迁移。

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