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氧化应激诱导生长抑制剂1（OSGIN1）是X盒结合蛋白1的一个靶点，通过维持自噬保护棕榈酸诱导的血管脂毒性。

Oxidative Stress-Induced Growth Inhibitor (OSGIN1), a Target of X-Box-Binding Protein 1, Protects Palmitic Acid-Induced Vascular Lipotoxicity through Maintaining Autophagy.

作者信息

Khoi Chong-Sun, Xiao Cai-Qin, Hung Kuan-Yu, Lin Tzu-Yu, Chiang Chih-Kang

机构信息

Graduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei 106, Taiwan.

Department of Anesthesiology, Far-Eastern Memorial Hospital, New Taipei City 22060, Taiwan.

出版信息

Biomedicines. 2022 Apr 25;10(5):992. doi: 10.3390/biomedicines10050992.

DOI:10.3390/biomedicines10050992
PMID:35625730
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9138516/
Abstract

Saturated free fatty acids (FFAs) strongly correlate with metabolic syndromes and are well-known risk factors for cardiovascular diseases (CVDs). The mechanism of palmitic acid (PA)-induced vascular lipotoxicity under endoplasmic reticulum (ER) stress is unknown. In the present paper, we investigate the roles of spliced form of X-box-binding protein 1 (XBP1s) target gene oxidative stress-induced growth inhibitor 1 (OSGIN1) in PA-induced vascular dysfunction. PA inhibited the tube formation assay of primary human umbilical vein endothelial cells (HUVECs). Simultaneously, PA treatment induced the XBP1s expression in HUVECs. Attenuate the induction of XBP1s by silencing the XBP1s retarded cell migration and diminished endothelial nitric oxide synthase (eNOS) expression. OSGIN1 is a target gene of XBP1s under PA treatment. The silencing of OSGIN1 inhibits cell migration by decreasing phospho-eNOS expression. PA activated autophagy in endothelial cells, inhibiting autophagy by 3-methyladenine (3-MA) decreased endothelial cell migration. Silencing XBP1s and OSGIN1 would reduce the induction of LC3 II; therefore, OSGIN1 could maintain autophagy to preserve endothelial cell migration. In conclusion, PA treatment induced ER stress and activated the inositol-requiring enzyme 1 alpha-spliced XBP1 (IRE1α-XBP1s) pathway. OSGIN1, a target gene of XBP1s, could protect endothelial cells from vascular lipotoxicity by regulating autophagy.

摘要

饱和游离脂肪酸（FFAs）与代谢综合征密切相关，是心血管疾病（CVDs）的众所周知的危险因素。内质网（ER）应激下棕榈酸（PA）诱导血管脂毒性的机制尚不清楚。在本文中，我们研究了X盒结合蛋白1剪接形式（XBP1s）的靶基因氧化应激诱导生长抑制因子1（OSGIN1）在PA诱导的血管功能障碍中的作用。PA抑制原代人脐静脉内皮细胞（HUVECs）的管腔形成实验。同时，PA处理诱导HUVECs中XBP1s的表达。通过沉默XBP1s减弱其诱导作用会阻碍细胞迁移并降低内皮型一氧化氮合酶（eNOS）的表达。OSGIN1是PA处理下XBP1s的靶基因。沉默OSGIN1通过降低磷酸化eNOS的表达来抑制细胞迁移。PA激活内皮细胞中的自噬，用3-甲基腺嘌呤（3-MA）抑制自噬会降低内皮细胞迁移。沉默XBP1s和OSGIN1会减少LC3 II的诱导；因此，OSGIN1可以维持自噬以保持内皮细胞迁移。总之，PA处理诱导内质网应激并激活肌醇需求酶1α剪接的XBP1（IRE1α-XBP1s）途径。OSGIN1作为XBP1s的靶基因，可以通过调节自噬保护内皮细胞免受血管脂毒性。

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