Ethanol causes the redistribution of L1 cell adhesion molecule in lipid rafts.
Ethanol causes the redistribution of L1 cell adhesion molecule in lipid rafts.
复制标题
乙醇导致 L1 细胞粘附分子在脂筏中重新分布。
DOI：
10.1111/j.1471-4159.2011.07467.x
复制
发表时间：
2011
影响因子：
4.7
通讯作者：
Bearer,CynthiaF
中科院分区：
文献类型：
--
作者：
Tang,Ningfeng;Farah,Benjamin;He,Min;Fox,Stephanie;Malouf,Alfred;Littner,Yoav;Bearer,CynthiaF
J. Neurochem.(2011)119, 859–867.AbstractFetal alcohol spectrum disorder is estimated to affect 1% of live births. The similarities between children with fetal alcohol syndrome and those with mutations in the gene encoding L1 cell adhesion molecule (L1) implicates L1 as a target of ethanol developmental neurotoxicity. Ethanol specifically inhibits the neurite outgrowth promoting function of L1 at pharmacologic concentrations. Emerging evidence shows that localized disruption of the lipid rafts reduces L1‐mediated neurite outgrowth. We hypothesize that ethanol impairment of the association of L1 with lipid rafts is a mechanism underlying ethanol’s inhibition of L1‐mediated neurite outgrowth. In this study, we examine the effects of ethanol on the association of L1 and lipid rafts. We show that,in vitro, L1 but not N‐cadherin shifts into lipid rafts following treatment with 25 mM ethanol. The ethanol concentrations causing this effect are similar to those inhibiting L1‐mediated neurite outgrowth. Increasing chain length of the alcohol demonstrates the same cutoff as that previously shown for inhibition of L1–L1 binding. In addition, in cerebellar granule neurons in which lipid rafts are disrupted with methyl‐beta‐cyclodextrin, the rate of L1‐mediated neurite outgrowth on L1‐Fc is reduced to background rate and that this background rate is not ethanol sensitive. These data indicate that ethanol may inhibit L1‐mediated neurite outgrowth by retarding L1 trafficking through a lipid raft compartment.
