A Novel STAT3-Mediated GATA6 Pathway Contributes to tert-Butylhydroquinone- (tBHQ-) Protected TNFα-Activated Vascular Cell Adhesion Molecule 1 (VCAM-1) in Vascular Endothelium.
A Novel STAT3-Mediated GATA6 Pathway Contributes to tert-Butylhydroquinone- (tBHQ-) Protected TNFα-Activated Vascular Cell Adhesion Molecule 1 (VCAM-1) in Vascular Endothelium.
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一种新的STAT 3介导的GATA 6通路有助于在血管内皮细胞中保护叔丁基氢醌-（tBHQ-）TNFα激活的血管细胞粘附分子1（VCAM-1）。
DOI：
10.1155/2020/6584059
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发表时间：
2020
影响因子：
--
通讯作者：
Li S
中科院分区：
文献类型：
--
作者：
Zhou L;Ning H;Wei H;Xu T;Zhao X;Fu A;Qian Q;Yang Z;Dou X;Li S
The activation of vascular cell adhesion molecule 1 (VCAM-1) in vascular endothelial cells has been well considered implicating in the initiation and processing of atherosclerosis. Oxidative stress is mechanistically involved in proatherosclerotic cytokine-induced VCAM-1 activation. tert-Butylhydroquinone (tBHQ), a synthetic phenolic antioxidant used for preventing lipid peroxidation of food, possesses strongly antioxidant capacity against oxidative stress-induced dysfunction in various pathological process. Here, we investigated the protective role of tBHQ on tumor necrosis factor alpha- (TNFα-) induced VCAM-1 activation in both aortic endothelium of mice and cultured human vascular endothelial cells and uncovered its potential mechanisms. Our data showed that tBHQ treatment significantly reversed TNFα-induced activation of VCAM-1 at both transcriptional and protein levels. The mechanistic study revealed that inhibiting neither nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nor autophagy blocked the beneficial role of tBHQ. Alternatively, tBHQ intervention markedly alleviated TNFα-increased GATA-binding protein 6 (GATA6) mRNA and protein expressions and its translocation into nucleus. Further investigation indicated that tBHQ-inhibited signal transducer and activator of transcription 3 (STAT3) but not mitogen-activated protein kinase (MAPK) pathway contributed to its protective role against VCAM-1 activation via regulating GATA6. Collectively, our data demonstrated that tBHQ prevented TNFα-activated VCAM-1 via a novel STAT3/GATA6-involved pathway. tBHQ could be a potential candidate for the prevention of proatherosclerotic cytokine-caused inflammatory response and further dysfunctions in vascular endothelium.
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叔丁基氢醌 (tBHQ) 通过诱导自噬来保护肝细胞免受脂毒性，而与 Nrf2 激活无关。
DOI：
10.1016/j.bbalip.2013.09.004
发表时间：
2014-01
期刊：
Biochimica et biophysica acta
影响因子：
--
作者：
Li S;Li J;Shen C;Zhang X;Sun S;Cho M;Sun C;Song Z
通讯作者：
Song Z
影响因子：
4.6
作者：
Jin W;Ni H;Dai Y;Wang H;Lu T;Wu J;Jiang J;Liang W
通讯作者：
Liang W
影响因子：
20.1
作者：
Kobiyama K;Ley K
通讯作者：
Ley K
影响因子：
4.8
作者：
Kim, I;Moon, SO;Koh, GY
通讯作者：
Koh, GY
影响因子：
7.4
作者：
Duan, Xiaoxu;Li, Jinlong;Li, Bing
通讯作者：
Li, Bing