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ABCA1介导的高密度脂蛋白(HDL)形成所需的细胞磷脂酰链的结构特征。

The structural characteristics of cellular phospholipid acyl chains required for ABCA1-mediated HDL formation.

作者信息

Nagao Kohjiro, Matsuo Mayu, Hori Yoshie, Namba Norihiro, Saito Hiroyuki

机构信息

Laboratory of Biophysical Chemistry, Kyoto Pharmaceutical University, Kyoto, Japan.

Laboratory of Biophysical Chemistry, Kyoto Pharmaceutical University, Kyoto, Japan.

出版信息

J Biol Chem. 2025 Jul 4;301(8):110457. doi: 10.1016/j.jbc.2025.110457.

Abstract

ATP-binding cassette protein A1 (ABCA1) mediates high-density lipoprotein (HDL) formation by transporting cellular cholesterol and phospholipids to apolipoprotein A-I (apoA-I). Although phospholipids serve as transport substrates for ABCA1, and the membrane constituents surrounding ABCA1, their roles in HDL formation remain unclear. Here, we elucidated the effect of the acyl chain structure of cellular phospholipids on HDL formation, particularly focusing on monounsaturated fatty acid (MUFA)-containing phosphatidylcholine (PC), the predominant phospholipid in most animal cells. PC molecules effluxed to apoA-I had an acyl chain composition similar to cellular PC, both being enriched in MUFA-containing species. Furthermore, manipulating the acyl chain composition of cellular PC by stealoyl-CoA desaturase inhibition or fatty acid supplementation led to similar changes in effluxed PC molecule composition. Thus, ABCA1 can transport various cellular PC molecules, including MUFA-containing species, without apparent preference for their acyl chain structure. Conversely, an appropriate acyl chain composition of cellular phospholipids is required for ABCA1 functional expression. Reducing MUFA content in the cellular phospholipids suppressed ABCA1 expression through two independent mechanisms: first, by inducing an endoplasmic reticulum (ER) stress response that decreases ABCA1 protein production; and second, by causing a folding defect in the ABCA1 protein, leading to immature glycosylation and failure of plasma membrane localization. Excess MUFA supply decreased ABCA1 expression without causing ER stress or defects in glycosylation and localization of ABCA1. Collectively, we revealed the contribution of MUFA-containing PC to HDL formation and identified the structural characteristics of cellular phospholipids required for their transport to apoA-I and functional expression of ABCA1.

摘要

ATP结合盒转运蛋白A1(ABCA1)通过将细胞内胆固醇和磷脂转运至载脂蛋白A-I(apoA-I)来介导高密度脂蛋白(HDL)的形成。尽管磷脂作为ABCA1的转运底物以及其周围的膜成分,但其在HDL形成中的作用仍不清楚。在此,我们阐明了细胞磷脂的酰基链结构对HDL形成的影响,特别关注大多数动物细胞中主要的磷脂——含单不饱和脂肪酸(MUFA)的磷脂酰胆碱(PC)。外流至apoA-I的PC分子的酰基链组成与细胞PC相似,二者均富含含MUFA的种类。此外,通过抑制硬脂酰辅酶A去饱和酶或补充脂肪酸来操纵细胞PC的酰基链组成,会导致外流PC分子组成发生类似变化。因此,ABCA1可以转运各种细胞PC分子,包括含MUFA的种类,而对其酰基链结构没有明显偏好。相反,细胞磷脂需要适当的酰基链组成才能实现ABCA1的功能性表达。降低细胞磷脂中的MUFA含量通过两种独立机制抑制ABCA1表达:第一,通过诱导内质网(ER)应激反应,减少ABCA1蛋白的产生;第二,通过导致ABCA1蛋白折叠缺陷,导致糖基化不成熟和质膜定位失败。过量供应MUFA会降低ABCA1表达,但不会引起ER应激或ABCA1糖基化及定位缺陷。总体而言,我们揭示了含MUFA的PC对HDL形成的贡献,并确定了细胞磷脂转运至apoA-I及其ABCA1功能性表达所需的结构特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1be9/12336828/614dd14dc277/gr1.jpg

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