Reactive oxygen species mediate oxidized low-density lipoprotein-induced endothelin-1 gene expression via extracellular signal-regulated kinase in vascular endothelial cells

Xu, Honghao; Duan, Jiaqi; Wang, Wen; Dai, Shunling; Wu, Yuwei; Sun, Renyu; Ren, Jun

doi:10.1097/hjh.0b013e3282f56bb7

Cited by 21 publications

(25 citation statements)

References 33 publications

(45 reference statements)

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“…It was demonstrated that a significant amount of ROS was produced spontaneously from ox-LDL at clinically relevant concentrations, and was involved in the action of ox-LDL on human umbilical vein endothelial cells [28,29], bone marrow (BM) stem cells [30], vascular smooth muscle cells [31], monocytes [32], macrophage [33] and foam cells [34]. Treatment with ox-LDL increased intracellular ROS generation in cultured endothelial cells [35].…”

Section: Introductionmentioning

confidence: 99%

Probucol Protects Endothelial Progenitor Cells Against Oxidized Low-Density Lipoprotein via Suppression of Reactive Oxygen Species Formation In Vivo

Zhang

Chen

et al. 2016

Cell Physiol Biochem

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Background/Aims: Oxidized low-density lipoprotein (ox-LDL) is a major component of hyperlipidemia and contributes to atherosclerosis. Endothelial progenitor cells (EPCs) play an important role in preventing atherosclerosis and notably decreased in hyperlipidemia. Ox-LDL and ox-LDL-related reactive oxygen species (ROS) have deleterious effects on EPCs. Probucol as an antioxidant and anti-inflammatory drug reduces ROS production. The present study was to determine if probucol could protect EPCs from ox-LDL in vivo and to investigate the potential mechanisms. Methods: ox-LDL was injected into male C57BL/6 mice for 3 days with or without probucol treatment with PBS as control. Bone marrow (BM) fluid, serum, circulating mononuclear cells (MNCs) and EPCs were collected for analysis. Results: the increased extracellular ROS in BM, serum and blood intracellular ROS production in the mice with ox-LDL treatment in association with a significant reduction of circulating MNCs and EPCs were restored with Probucol treatment. A significant increase in the serum ox-LDL and C-reactive protein and decrease in superoxide dismutase and circulating MNCs and EPCs were observed in hyperlipidemic patients that were effectively reversed with probucol treatment. Conclusion: these data suggested that probucol could protect EPCs from ox-LDL through inhibition of ROS production in vivo.

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Section: Introductionmentioning

confidence: 99%

Probucol Protects Endothelial Progenitor Cells Against Oxidized Low-Density Lipoprotein via Suppression of Reactive Oxygen Species Formation In Vivo

Zhang

Chen

et al. 2016

Cell Physiol Biochem

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“…No doubt antiinfl ammatory actions of resveratrol in this event should be able to delay or prevent endothelial dysfunctions induced by LPC. ERK, a subfamily of the mitogen-activated protein kinases (MAPK), has been reported that its activation induced by LPC in the endothelium plays a key role in evoking infl ammation and potentiating vessel contractive responses (Bochkov et al, 2002;Xu et al, 2008;Suenaga and Kamata, 2003;Matsumoto et al, 2006). In the present study, PD 98059 exerted signifi cant vasculoprotection by suppressing the local induction of infl ammatory genes and reversing LPC-induced vasoconstriction, further confi rming that ERK-activation was associated with LPC-induced endothelial dysfunction in this preparation, and elucidating a possible link between endothelial infl ammation and loss of EDR.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol restores lysophosphatidylcholine‐induced loss of endothelium‐dependent relaxation in rat aorta tissue coinciding with inhibition of extracellular‐signal‐regulated protein kinase activation

Zhang

Liu

Lin

et al. 2010

Phytotherapy Research

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To investigate whether resveratrol could restore the lysophosphatidylcholine (LPC)-induced loss of endothelium-dependent relaxation in in vitro cultured rat aorta tissue, first the effect of resveratrol on the loss of EDR was examined in this preparation. The results showed that resveratrol effectively attenuated the inhibition of LPC (10 μM) on both endothelium-derived relaxing factor (EDRF) and endothelium-derived hyperpolarizing factor (EDHF) in a concentration-dependent manner (1, 10, 100 μM). In addition, resveratrol inhibited elevated K+-induced vascular contracture, but had no significant effects on ACh (1 μM)-induced endothelium-dependent relaxation (EDR). A similar tendency was also observed with PD 98059 (30 μM), a selective inhibitor of ERK. When the cells were exposed to LPC (20 μM) the mRNA expression of eNOS and COX-1 mRNA were down-regulated, followed by a local induction of iNOS and COX-2. Resveratrol and PD 98059 successfully reversed the effects of LPC on relative mRNA expressions. Both resveratrol and PD 98059 inhibited the activation of ERK induced by LPC. These findings demonstrate that resveratrol can restore the LPC-induced loss of EDR in rat aorta and protect the endothelium against LPC-induced injuries via the inhibition of the inflammation-like response.

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“…Besides, NAD(P)H oxidase pathway, dysfunction of endothelium, and vascular remodeling can be the result of an activated extracellular signal–regulated kinases (ERK) signaling pathway. Numerous studies have shown that increased level of oxLDL induces accumulation of ROS, which stimulates ERK phosphorylation, upregulates the expression of endothelial transcriptional factor AP‐1 and ET‐1, and, consequently, promotes the progression of atherosclerosis …”

Section: Redox Signaling In the Vascular Pathophysiologymentioning

confidence: 99%

Redox control of vascular biology

et al. 2019

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Redox control is lost when the antioxidant defense system cannot remove abnormally high concentrations of signaling molecules, such as reactive oxygen species (ROS). Chronically elevated levels of ROS cause oxidative stress that may eventually lead to cancer and cardiovascular and neurodegenerative diseases. In this review, we focus on redox effects in the vascular system. We pay close attention to the subcompartments of the vascular system (endothelium, smooth muscle cell layer) and give an overview of how redox changes influence those different compartments. We also review the core aspects of redox biology, cardiovascular physiology, and pathophysiology. Moreover, the topic‐specific knowledgebase DES‐RedoxVasc was used to develop two case studies, one focused on endothelial cells and the other on the vascular smooth muscle cells, as a starting point to possibly extend our knowledge of redox control in vascular biology.

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Reactive oxygen species mediate oxidized low-density lipoprotein-induced endothelin-1 gene expression via extracellular signal-regulated kinase in vascular endothelial cells

Abstract: Collectively, our data favor the notion that oxLDL stimulates ERK phosphorylation via ROS accumulation, which in turn stimulates vascular endothelial transcriptional factor activator protein-1 and ET-1 expression as well as secretion.

Cited by 21 publications

References 33 publications

Probucol Protects Endothelial Progenitor Cells Against Oxidized Low-Density Lipoprotein via Suppression of Reactive Oxygen Species Formation In Vivo

Probucol Protects Endothelial Progenitor Cells Against Oxidized Low-Density Lipoprotein via Suppression of Reactive Oxygen Species Formation In Vivo

Resveratrol restores lysophosphatidylcholine‐induced loss of endothelium‐dependent relaxation in rat aorta tissue coinciding with inhibition of extracellular‐signal‐regulated protein kinase activation

Redox control of vascular biology

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