Role of thioredoxin-interacting protein in mediating endothelial dysfunction in hypertension

Excessive oxidative stress is a major causative factor of endothelial dysfunction in hypertension. As an endogenous pro-oxidant, thioredoxin-interacting protein (TXNIP) contributes to oxidative damage in various tissues. The present study aimed to investigate the role of TXNIP in mediating endotheli...

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Published in:	Genes & diseases Vol. 9; no. 3; pp. 753 - 765
Main Authors:	Wang, Ruiyu, Guo, Yongzheng, Li, Lingjiao, Luo, Minghao, Peng, Linqian, Lv, Dingyi, Cheng, Zhe, Xue, Qian, Wang, Liang, Huang, Jing
Format:	Journal Article
Language:	English
Published:	Elsevier B.V 01.05.2022 Chongqing Medical University KeAi Communications Co., Ltd
Subjects:	Endothelial dysfunction eNOS Full Length Hypertension Oxidative stress Thioredoxin-interacting protein Hypertension Endothelial dysfunction Oxidative stress eNOS Thioredoxin-interacting protein
ISSN:	2352-3042, 2352-4820, 2352-3042
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Abstract	Excessive oxidative stress is a major causative factor of endothelial dysfunction in hypertension. As an endogenous pro-oxidant, thioredoxin-interacting protein (TXNIP) contributes to oxidative damage in various tissues. The present study aimed to investigate the role of TXNIP in mediating endothelial dysfunction in hypertension. In vivo, an experimental model of acquired hypertension was established with two-kidney, one-clip (2K1C) surgery. The expression of TXNIP in the vascular endothelial cells of multiple vessels was significantly increased in hypertensive rats compared with sham-operated rats. Resveratrol, a TXNIP inhibitor, suppressed vascular oxidative damage and increased the expression and activity of eNOS in the aorta of hypertensive rats. Notably, impaired endothelium-dependent vasodilation was effectively improved by TXNIP inhibition in hypertensive rats. In vitro, we observed that Ang II increased the expression of TXNIP in primary human aortic endothelial cells (HAECs) and that TXNIP knockdown by RNA interference alleviated cellular oxidative stress damage and mitigated the impaired eNOS activation and intracellular nitric oxide (NO) production observed in Ang II-treated HAECs. However, inhibiting thioredoxin (TRX) with PX-12 completely blunted the protective effect of silencing TXNIP. In addition, TXNIP knockdown facilitated TRX expression and promoted TRX nuclear translocation to further activate AP1 and REF1. TRX overexpression exhibited favorable effects on eNOS/NO homeostasis in Ang II-treated HAECs. Thus, TXNIP contributes to oxidative stress and endothelial dysfunction in hypertension, and these effects are dependent on the antioxidant capacity of TRX, suggesting that targeting TXNIP may be a novel strategy for antihypertensive therapy.
AbstractList	Excessive oxidative stress is a major causative factor of endothelial dysfunction in hypertension. As an endogenous pro-oxidant, thioredoxin-interacting protein (TXNIP) contributes to oxidative damage in various tissues. The present study aimed to investigate the role of TXNIP in mediating endothelial dysfunction in hypertension. In vivo, an experimental model of acquired hypertension was established with two-kidney, one-clip (2K1C) surgery. The expression of TXNIP in the vascular endothelial cells of multiple vessels was significantly increased in hypertensive rats compared with sham-operated rats. Resveratrol, a TXNIP inhibitor, suppressed vascular oxidative damage and increased the expression and activity of eNOS in the aorta of hypertensive rats. Notably, impaired endothelium-dependent vasodilation was effectively improved by TXNIP inhibition in hypertensive rats. In vitro, we observed that Ang II increased the expression of TXNIP in primary human aortic endothelial cells (HAECs) and that TXNIP knockdown by RNA interference alleviated cellular oxidative stress damage and mitigated the impaired eNOS activation and intracellular nitric oxide (NO) production observed in Ang II-treated HAECs. However, inhibiting thioredoxin (TRX) with PX-12 completely blunted the protective effect of silencing TXNIP. In addition, TXNIP knockdown facilitated TRX expression and promoted TRX nuclear translocation to further activate AP1 and REF1. TRX overexpression exhibited favorable effects on eNOS/NO homeostasis in Ang II-treated HAECs. Thus, TXNIP contributes to oxidative stress and endothelial dysfunction in hypertension, and these effects are dependent on the antioxidant capacity of TRX, suggesting that targeting TXNIP may be a novel strategy for antihypertensive therapy. Excessive oxidative stress is a major causative factor of endothelial dysfunction in hypertension. As an endogenous pro-oxidant, thioredoxin-interacting protein (TXNIP) contributes to oxidative damage in various tissues. The present study aimed to investigate the role of TXNIP in mediating endothelial dysfunction in hypertension. In vivo, an experimental model of acquired hypertension was established with two-kidney, one-clip (2K1C) surgery. The expression of TXNIP in the vascular endothelial cells of multiple vessels was significantly increased in hypertensive rats compared with sham-operated rats. Resveratrol, a TXNIP inhibitor, suppressed vascular oxidative damage and increased the expression and activity of eNOS in the aorta of hypertensive rats. Notably, impaired endothelium-dependent vasodilation was effectively improved by TXNIP inhibition in hypertensive rats. In vitro, we observed that Ang II increased the expression of TXNIP in primary human aortic endothelial cells (HAECs) and that TXNIP knockdown by RNA interference alleviated cellular oxidative stress damage and mitigated the impaired eNOS activation and intracellular nitric oxide (NO) production observed in Ang II-treated HAECs. However, inhibiting thioredoxin (TRX) with PX-12 completely blunted the protective effect of silencing TXNIP. In addition, TXNIP knockdown facilitated TRX expression and promoted TRX nuclear translocation to further activate AP1 and REF1. TRX overexpression exhibited favorable effects on eNOS/NO homeostasis in Ang II-treated HAECs. Thus, TXNIP contributes to oxidative stress and endothelial dysfunction in hypertension, and these effects are dependent on the antioxidant capacity of TRX, suggesting that targeting TXNIP may be a novel strategy for antihypertensive therapy.Excessive oxidative stress is a major causative factor of endothelial dysfunction in hypertension. As an endogenous pro-oxidant, thioredoxin-interacting protein (TXNIP) contributes to oxidative damage in various tissues. The present study aimed to investigate the role of TXNIP in mediating endothelial dysfunction in hypertension. In vivo, an experimental model of acquired hypertension was established with two-kidney, one-clip (2K1C) surgery. The expression of TXNIP in the vascular endothelial cells of multiple vessels was significantly increased in hypertensive rats compared with sham-operated rats. Resveratrol, a TXNIP inhibitor, suppressed vascular oxidative damage and increased the expression and activity of eNOS in the aorta of hypertensive rats. Notably, impaired endothelium-dependent vasodilation was effectively improved by TXNIP inhibition in hypertensive rats. In vitro, we observed that Ang II increased the expression of TXNIP in primary human aortic endothelial cells (HAECs) and that TXNIP knockdown by RNA interference alleviated cellular oxidative stress damage and mitigated the impaired eNOS activation and intracellular nitric oxide (NO) production observed in Ang II-treated HAECs. However, inhibiting thioredoxin (TRX) with PX-12 completely blunted the protective effect of silencing TXNIP. In addition, TXNIP knockdown facilitated TRX expression and promoted TRX nuclear translocation to further activate AP1 and REF1. TRX overexpression exhibited favorable effects on eNOS/NO homeostasis in Ang II-treated HAECs. Thus, TXNIP contributes to oxidative stress and endothelial dysfunction in hypertension, and these effects are dependent on the antioxidant capacity of TRX, suggesting that targeting TXNIP may be a novel strategy for antihypertensive therapy.
Author	Guo, Yongzheng Cheng, Zhe Xue, Qian Lv, Dingyi Li, Lingjiao Huang, Jing Luo, Minghao Wang, Liang Wang, Ruiyu Peng, Linqian
Author_xml	– sequence: 1 givenname: Ruiyu surname: Wang fullname: Wang, Ruiyu organization: Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, PR China – sequence: 2 givenname: Yongzheng surname: Guo fullname: Guo, Yongzheng organization: Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China – sequence: 3 givenname: Lingjiao surname: Li fullname: Li, Lingjiao organization: Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, PR China – sequence: 4 givenname: Minghao surname: Luo fullname: Luo, Minghao organization: Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China – sequence: 5 givenname: Linqian surname: Peng fullname: Peng, Linqian organization: Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China – sequence: 6 givenname: Dingyi surname: Lv fullname: Lv, Dingyi organization: Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China – sequence: 7 givenname: Zhe surname: Cheng fullname: Cheng, Zhe organization: Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China – sequence: 8 givenname: Qian surname: Xue fullname: Xue, Qian organization: Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, PR China – sequence: 9 givenname: Liang surname: Wang fullname: Wang, Liang organization: Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, PR China – sequence: 10 givenname: Jing surname: Huang fullname: Huang, Jing email: huangjing@cqmu.edu.cn organization: Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, PR China
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SubjectTerms	Endothelial dysfunction eNOS Full Length Hypertension Oxidative stress Thioredoxin-interacting protein
Title	Role of thioredoxin-interacting protein in mediating endothelial dysfunction in hypertension
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