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ABCG1 通过抑制 NADPH 氧化酶和上调 Nrf2 介导的抗氧化防御来减轻 HO 引起的氧化应激在血管内皮细胞中。

ABCG1 Attenuates Oxidative Stress Induced by HO through the Inhibition of NADPH Oxidase and the Upregulation of Nrf2-Mediated Antioxidant Defense in Endothelial Cells.

机构信息

Department of Cardiovascular Medicine, Second Affiliated Hospital of Xi'an Jiaotong University, 157 West Five Road, Xi'an, Shaanxi 710004, China.

出版信息

Anal Cell Pathol (Amst). 2020 Dec 3;2020:2095645. doi: 10.1155/2020/2095645. eCollection 2020.

DOI:10.1155/2020/2095645
PMID:33344146
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7732382/
Abstract

. Oxidative stress is an important factor that is related to endothelial dysfunction. ATP-binding cassette transporter G1 (ABCG1), a regulator of intracellular cholesterol efflux, has been found to prevent endothelial activation in vessel walls. To explore the role of ABCG1 in oxidative stress production in endothelial cells, HUAECs were exposed to HO and transfected with the specific ABCG1 siRNA or ABCG1 overexpression plasmid. The results showed that overexpression of ABCG1 by ABCG1 plasmid or liver X receptor (LXR) agonist T0901317 treatment inhibited ROS production and MDA content induced by HO in HUAECs. Furthermore, ABCG1 upregulation blunted the activity of prooxidant NADPH oxidase and the expression of Nox4, one of the NADPH oxidase subunits. Moreover, the increased migration of Nrf2 from the cytoplasm to the nucleus and antioxidant HO-1 expression were detected in HUAECs with upregulation of ABCG1. Conversely, ABCG1 downregulation by ABCG1 siRNA increased NADPH oxidase activity and Nox4 expression and abrogated the increase at Nrf2 nuclear protein levels. In addition, intracellular cholesterol load interfered with the balance between NADPH oxidase activity and HO-1 expression. It was suggested that ABCG1 attenuated oxidative stress induced by HO in endothelial cells, which might be involved in the balance between decreased NADPH oxidase activity and increased Nrf2/OH-1 antioxidant defense signaling via its regulation for intracellular cholesterol accumulation.

摘要

氧化应激是与内皮功能障碍相关的重要因素。ATP 结合盒转运体 G1（ABCG1）是细胞内胆固醇流出的调节剂，已被发现可防止血管壁内皮细胞的激活。为了探讨 ABCG1 在内皮细胞氧化应激产生中的作用，将 HUAEC 暴露于 HO 并转染特异性 ABCG1 siRNA 或 ABCG1 过表达质粒。结果表明，ABCG1 质粒过表达或肝 X 受体（LXR）激动剂 T0901317 处理抑制了 HO 诱导的 HUAECs 中 ROS 产生和 MDA 含量。此外，ABCG1 的上调减弱了促氧化剂 NADPH 氧化酶的活性和 NADPH 氧化酶亚基之一 Nox4 的表达。此外，在 ABCG1 过表达的 HUAECs 中检测到 Nrf2 从细胞质向细胞核的迁移增加和抗氧化 HO-1 的表达。相反，ABCG1 siRNA 下调通过 ABCG1 增加 NADPH 氧化酶活性和 Nox4 表达并消除 Nrf2 核蛋白水平的增加。此外，细胞内胆固醇负荷干扰了 NADPH 氧化酶活性和 HO-1 表达之间的平衡。这表明 ABCG1 减轻了 HO 诱导的内皮细胞中的氧化应激，这可能涉及通过其对细胞内胆固醇积累的调节来降低 NADPH 氧化酶活性和增加 Nrf2/HO-1 抗氧化防御信号之间的平衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/795bc2c81588/ACP2020-2095645.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/59d3265a37da/ACP2020-2095645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/177927caa4bc/ACP2020-2095645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/b9e256cbe57c/ACP2020-2095645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/c8fe1f0c218c/ACP2020-2095645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/795bc2c81588/ACP2020-2095645.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/59d3265a37da/ACP2020-2095645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/177927caa4bc/ACP2020-2095645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/b9e256cbe57c/ACP2020-2095645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/c8fe1f0c218c/ACP2020-2095645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba6b/7732382/795bc2c81588/ACP2020-2095645.005.jpg

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