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阿朴酯素通过与 IRE1α 结合保护内皮细胞免受内质网应激诱导的细胞凋亡。

Apocynin protects endothelial cells from endoplasmic reticulum stress-induced apoptosis via IRE1α engagement.

机构信息

The First School of Clinical Medicine, Southern Medical University, Guangzhou, China.

Department of Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, China.

出版信息

Mol Cell Biochem. 2018 Dec;449(1-2):257-265. doi: 10.1007/s11010-018-3362-4. Epub 2018 Apr 25.

DOI:10.1007/s11010-018-3362-4
PMID:29696609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7088535/
Abstract

Endoplasmic reticulum (ER) stress-induced endothelial cell (EC) apoptosis has been implicated in a variety of human diseases. In addition to being regarded as an NADPH oxidase (NOX) inhibitor, apocynin (APO) exhibits an anti-apoptotic effect in various cells. The present study aimed to identify the protective role of apocynin in ER stress-mediated EC apoptosis and the underlying mechanisms. We found that ER stress resulted in a significant increase in c-Jun N-terminal kinase phosphorylation, and elicited caspase 3 cleavage and apoptosis. However, apocynin obviously attenuated EC apoptosis and this effect was partly dependent on ER stress sensor inositol-requiring enzyme 1α (IRE1α). Importantly, apocynin upregulated IRE1α expression in both protein and mRNA levels and promoted the pro-survival XBP1 splicing. Our results suggest that apocynin protects ECs against ER stress-induced apoptosis via IRE1α involvement. These findings may provide a novel mechanistic explanation for the anti-apoptotic effect of apocynin in ER stress.

摘要

内质网（ER）应激诱导的内皮细胞（EC）凋亡与多种人类疾病有关。除了被认为是 NADPH 氧化酶（NOX）抑制剂外，育亨宾（APO）在各种细胞中表现出抗凋亡作用。本研究旨在确定育亨宾在 ER 应激介导的 EC 凋亡中的保护作用及其潜在机制。我们发现 ER 应激导致 c-Jun N 末端激酶磷酸化显著增加，并引发 caspase 3 切割和凋亡。然而，育亨宾明显减轻了 EC 凋亡，这种作用部分依赖于内质网应激传感器肌醇需求酶 1α（IRE1α）。重要的是，育亨宾在蛋白和 mRNA 水平上均上调 IRE1α 的表达，并促进了生存促进的 XBP1 剪接。我们的研究结果表明，育亨宾通过 IRE1α 的参与保护 EC 免受 ER 应激诱导的凋亡。这些发现可能为育亨宾在 ER 应激中的抗凋亡作用提供新的机制解释。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/4dc14039b189/11010_2018_3362_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/3a14b9c38eee/11010_2018_3362_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/0b76c158e565/11010_2018_3362_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/fee3f66b425b/11010_2018_3362_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/325a3e742695/11010_2018_3362_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/4dc14039b189/11010_2018_3362_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/3a14b9c38eee/11010_2018_3362_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/0b76c158e565/11010_2018_3362_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/fee3f66b425b/11010_2018_3362_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/325a3e742695/11010_2018_3362_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3a7/7088535/4dc14039b189/11010_2018_3362_Fig5_HTML.jpg

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