scholarly journals Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium

2016 ◽  
Vol 7 ◽  
Author(s):  
Wenwen Zhao ◽  
Chunxia Li ◽  
Hongwei Gao ◽  
Qin Wu ◽  
Jingshan Shi ◽  
...  
Keyword(s):  
Oxidized Ldl ◽  
Ldl Receptor ◽  
Deficient Mice

F(ab′)2 fragments of anti-oxidized LDL IgG attenuate vascular inflammation and atherogenesis in diabetic LDL receptor-deficient mice

2016 ◽  
Vol 173 ◽  
pp. 50-56 ◽  
Author(s):  
Yanchun Li ◽  
Zhongyang Lu ◽  
Yan Huang ◽  
Maria F. Lopes-Virella ◽  
Gabriel Virella
Keyword(s):  
Oxidized Ldl ◽  
Vascular Inflammation ◽  
Ldl Receptor ◽  
Deficient Mice

scholarly journals Oxidized LDL but not angiotensin II induces the interaction between LOX-1 and AT1 receptors

2020 ◽  
Author(s):  
Li Lin ◽  
Ning Zhou ◽  
Le Kang ◽  
Qi Wang ◽  
Jian Wu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Direct Interaction ◽  
Cardiomyocyte Hypertrophy ◽  
Oxidized Low Density Lipoprotein ◽  
Protein Activation

Oxidized low-density lipoprotein (Ox-LDL) can induce cardiac hypertrophy, but the mechanism is still unclear. Here we elucidate the role of angiotensin II (AngII) receptor (AT1-R) in Ox-LDL-induced cardiomycyte hypertrophy. Inhibition of Ox-LDL receptor LOX-1 and AT1-R rather than AngII abolished Ox-LDL-induced hypertrophic responses. Similar results were obtained from the heart of mice lacking endogenous Ang II and their cardiomyocytes. Ox-LDL but not AngII induced binding of LOX-1 to AT1-R, and the inhibition of LOX-1 or AT1-R rather than AngII abolished the association of these two receptors. Ox-LDL-induced ERKs phosphorylation in LOX-1 and AT1-R-overexpression cells and the binding of both receptors were suppressed by the mutants of LOX-1 (Lys266Ala/Lys267Ala) or AT1-R (Glu257Ala), however, the AT1-R mutant lacking Gq protein-coupling ability only abolished the ERKs phosphorylation. The phosphorylation of ERKs induced by Ox-LDL in LOX-1 and AT1-R-overexpression cells was abrogated by Gq protein inhibitor but not by Jak2, Rac1 and RhoA inhibitors. Therefore, the direct interaction between LOX-1 and AT1-R and the downstream Gq protein activation are important mechanisms for Ox-LDL- but not AngII-induced cardiomyocyte hypertrophy

scholarly journals Role of Lectin-Like Oxidized Low Density Lipoprotein-1 in Fetoplacental Vascular Dysfunction in Preeclampsia

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Felipe A. Zuniga ◽  
Valeska Ormazabal ◽  
Nicolas Gutierrez ◽  
Valeria Aguilera ◽  
Claudia Radojkovic ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Vascular Dysfunction ◽  
Pathological Condition ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Fetal Loss ◽  
Density Lipoprotein ◽  
Placental Tissue

The bioavailability of nitric oxide (NO) represents a key marker in vascular health. A decrease in NO induces a pathological condition denominated endothelial dysfunction, syndrome observed in different pathologies, such as obesity, diabetes, kidney disease, cardiovascular disease, and preeclampsia (PE). PE is one of the major risks for maternal death and fetal loss. Recent studies suggest that the placenta of pregnant women with PE express high levels of lectin-like oxidized LDL receptor-1 (LOX-1), which induces endothelial dysfunction by increasing reactive oxygen species (ROS) and decreasing intracellular NO. Besides LOX-1 activation induces changes in migration and apoptosis of syncytiotrophoblast cells. However, the role of this receptor in placental tissue is still unknown. In this review we will describes the physiological roles of LOX-1 in normal placenta development and the potential involvement of this receptor in the pathophysiology of PE.

Abstract 621: Attenuated Expression of Profilin-1 Confers Protection from Atherosclerosis in the LDL Receptor-null Mouse

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Giulio R Romeo ◽  
Karen S Moulton ◽  
Andrius Kazlauskas
Keyword(s):  
Oxidized Ldl ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Normal Diet ◽  
Actin Binding ◽  
High Cholesterol Diet ◽  
Null Mouse ◽  
No Production ◽  
Descending Aorta

INTRODUCTION. Atherosclerosis-related events are a major cause of morbidity and death worldwide. The mechanisms underlying atherogenesis are not fully understood. We showed in previous studies that the actin-binding protein profilin-1 (pfn) was upregulated in atheroscle-rotic lesions and in endothelial cells (EC) treated with oxidized LDL (oxLDL). HYPOTHESIS. In the present study, we tested the hypothesis that pfn levels play a role in early atheroma formation. RESULTS. Since Pfn −/− mice die during embryonic development, we tested the role of pfn in atherogenesis by crossing adult Pfn +/− mice, which are viable and display a ∼50% reduction in pfn levels, into the Ldlr −/− mouse model of atherosclerosis. Atherosclerotic lesion burden was assessed in Pfn +/−Ldlr −/− (PfnHet) and Ldlr −/−control mice (PfnWT) fed an atherogenic high-cholesterol diet (HCD) for two months. Both males and females PfnHet exhibited a significant reduction in the percent lesion area in the descending aorta, when compared to PfnWT (females: 1.1 Â 27> 0.1 vs PfnWT 4.17 Â27> 0.49%, n=10; males: 1.34 Â 27> 0.22 vs PfnWT 3.4 Â 27> 0.36%, n=6). Similarly, aortic arch lesions were reduced in PfnHet (0.08 Â 27> 0.3 vs PfnWT 0.20 Â 27> 0.05 mm2, n=10). Total cholesterol and triglyceride levels were comparable in the two groups. Relevant atheroprotective changes were identified in PfnHet. When compared to PfnWT, aortas from PfnHet mice showed preserved eNOS activation, NO production and NO-dependent signaling. These changes were observed under HCD but not under a normal diet, thus indicating that pfn levels modified the response of the endothelium to atherogenic injury rather than its basal function. Similarly, knockdown of pfn in cultured aortic EC was protective against endothelial dysfunction triggered by oxLDL. Also, bone marrow-derived macrophages from PfnHet showed reduced internalization of oxLDL and oxLDL-induced inflammatory pathways, including activation of p38. CONCLUSIONS. These studies demonstrate that pfn levels modulate critical processes for atherosclerotic lesion formation through combined endothelial- and macrophage-dependent mechanisms.

scholarly journals The role of CD36 as an oxidized LDL receptor on atherogenesis

1998 ◽  
Vol 26 (1) ◽  
pp. 29-32
Author(s):  
Shuichi NOZAKI ◽  
Shizuya YAMASHITA ◽  
Yoshiaki TOMIYAMA ◽  
Yuji MATSUZAWA
Keyword(s):  
Oxidized Ldl ◽  
Ldl Receptor
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