Oxidized High-Density Lipoprotein Impairs Endothelial Progenitor Cells' Function by Activation of CD36-MAPK-TSP-1 Pathways

Wu, Ji; He, Zhiqing; Gao, Xiang; Wu, Feng; Ding, Ru; Ren, Yusheng; Jiang, Qijun; Fan, Min; Liang, Chun; Wu, Zonggui

doi:10.1089/ars.2013.5743

Cited by 25 publications

(23 citation statements)

References 75 publications

(81 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Probucol prevents LDL oxidation [85,86], increases SOD level and activity [87], decreases the levels of ox-LDL and CRP [72]. Probucol has been reported to rescue cigarette smoke-induced impairment of ischemiainduced neovascularization by improving the function of EPCs [48], and protect EPCs from oxidized high-density lipoprotein (ox-HDL) [49]. Additionally, it has been reported that probucol is able to prevent ROS-induced inactivation of endothelium-derived NO [88], reduce endogenous NO synthase inhibitor [43], and increase the level and function of NO, which could regulate the self-renewal, viability, migration, proliferation, and differentiation of EPCs [89].…”

Section: Discussionmentioning

confidence: 99%

“…Impaired ischemia-induced neovascularization by cigarette smoke could also be rescued by probucol via improved function of EPCs [48]. Probucol treatment could also protect EPCs from oxidized high-density lipoprotein (ox-HDL)-induced apoptosis [49]. The present study aimed to determine whether probucol could have protective effects on circulating MNCs and EPCs in mouse treated with ox-LDL and in hyperlipidemic patients with elevated ox-LDL level.…”

Section: Introductionmentioning

confidence: 95%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

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

View full text Add to dashboard Cite

show abstract

“…Angiogenetic activity of CD36 in endothelial cells is a result of its ability to activate specific cascade signal caused by proangiogenetic response directed to apoptotic response. 3,54,55 Muscle cells CD36 receptor is 85% homology with FAT/CD36 protein -fatty acid translocase. Its main role is cellular transportation of longchain fatty acids.…”

Section: Plateletsmentioning

confidence: 99%

The role of CD36 receptor in the pathogenesis of atherosclerosis

Choromańska¹,

Myśliwiec²,

Choromańska³

et al. 2017

Adv Clin Exp Med

View full text Add to dashboard Cite

“…However, the effect of peptides on TNF-and phorbol ester-induced inflammatory stimulation in various cells, including macrophages, was only marginally affected by SAHPs (54). Furthermore, recent data suggest that CD36 is one of the most important receptors associated with bacterial uptake, bacterial endotoxic cellular cytotoxicity (28), and acute and chronic kidney injury (28,(55)(56)(57). These recent data suggest that the vicious cycles of pathogen associated molecular pattern-induced inflammation and DAMP-induced tissue damage may well be mediated through CD36 (58,59).…”

Section: Discussionmentioning

confidence: 97%

Synthetic Amphipathic Helical Peptides Targeting CD36 Attenuate Lipopolysaccharide-Induced Inflammation and Acute Lung Injury

Bocharov

Baranova

et al. 2016

The Journal of Immunology

View full text Add to dashboard Cite

Synthetic amphipathic helical peptides (SAHPs) designed as apolipoprotein A-I mimetics are known to bind to class B scavenger receptors (SR-Bs), SR-BI, SR-BII, and CD36, receptors that mediate lipid transport and facilitate pathogen recognition. In this study, we evaluated SAHPs, selected for targeting human CD36, by their ability to attenuate LPS-induced inflammation, endothelial barrier dysfunction, and acute lung injury (ALI). L37pA, which targets CD36 and SR-BI equally, inhibited LPS-induced IL-8 secretion and barrier dysfunction in cultured endothelial cells while reducing lung neutrophil infiltration by 40% in a mouse model of LPS-induced ALI. A panel of 20 SAHPs was tested in HEK293 cell lines stably transfected with various SR-Bs to identify SAHPs with preferential selectivity toward CD36. Among several SAHPs targeting both SR-BI/BII and CD36 receptors, ELK-B acted predominantly through CD36. Compared with L37pA, 5A, and ELK SAHPs, ELK-B was most effective in reducing the pulmonary barrier dysfunction, neutrophil migration into the lung, and lung inflammation induced by LPS. We conclude that SAHPs with relative selectivity toward CD36 are more potent at inhibiting acute pulmonary inflammation and dysfunction. These data indicate that therapeutic strategies using SAHPs targeting CD36, but not necessarily mimicking all apolipoprotein A-I functions, may be considered a possible new treatment approach for inflammation-induced ALI and pulmonary edema.

show abstract

Oxidized High-Density Lipoprotein Impairs Endothelial Progenitor Cells' Function by Activation of CD36-MAPK-TSP-1 Pathways

Abstract: Activation of CD36-p38 MAPK-TSP-1 pathways contributes to the pathological effects of ox-HDL on EPCs' dysfunction, which might be one of the potential etiological factors responsible for the disturbed neovascularization in chronic ischemic disease.

Cited by 25 publications

References 75 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

The role of CD36 receptor in the pathogenesis of atherosclerosis

Synthetic Amphipathic Helical Peptides Targeting CD36 Attenuate Lipopolysaccharide-Induced Inflammation and Acute Lung Injury

Contact Info

Product

Resources

About