Angiotensin II increases the expression of lectin-like oxidized low-density lipoprotein receptor-1 in human vascular smooth muscle cells via a lipoxygenase-dependent pathway

Limor, Rona; Kaplan, Marielle; Sawamura, Tatsuya; Sharon, Orli; Keidar, Shlomo; Weisinger, Gary; Knoll, Esther; Naidich, Michal; Stern, Naftali

doi:10.1016/j.amjhyper.2004.09.008

Cited by 23 publications

(18 citation statements)

References 41 publications

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“…Since ox-LDL uptake through LOX-1 is critical for foam cell formation, which is the hallmark of the atherosclerotic region, and vSMCs in intimal area highly express LOX-1, some pioneer studies have addressed the role of vSMC related to LOX-1. Although these studies did not present direct evidence, high possibilities are suggested for the transformation from SMCs into foam cells though LOX-1 (42,43). Statins such as pravastatin showed a new pleiotropic effect, in which pravastatin downregulated LOX-1 expressions in human vSMCs and atherosclerotic lesions, and reduced intimal media thickness and lipid core area (43).…”

Section: The Role Of Membrane Receptors Of Vsmc In Vascular Inflammationmentioning

confidence: 93%

Role of vascular smooth muscle cell in the inflammation of atherosclerosis

Lim¹,

Park²

2014

BMB Reports

137

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Atherosclerosis is a pathologic process occurring within the artery, in which many cell types, including T cell, macrophages, endothelial cells, and smooth muscle cells, interact, and cause chronic inflammation, in response to various inner- or outer-cellular stimuli. Atherosclerosis is characterized by a complex interaction of inflammation, lipid deposition, vascular smooth muscle cell proliferation, endothelial dysfunction, and extracellular matrix remodeling, which will result in the formation of an intimal plaque. Although the regulation and function of vascular smooth muscle cells are important in the progression of atherosclerosis, the roles of smooth muscle cells in regulating vascular inflammation are rarely focused upon, compared to those of endothelial cells or inflammatory cells. Therefore, in this review, we will discuss here how smooth muscle cells contribute or regulate the inflammatory reaction in the progression of atherosclerosis, especially in the context of the activation of various membrane receptors, and how they may regulate vascular inflammation. [BMB Reports 2014; 47(1): 1-7]

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Section: The Role Of Membrane Receptors Of Vsmc In Vascular Inflammationmentioning

confidence: 93%

Role of vascular smooth muscle cell in the inflammation of atherosclerosis

Lim¹,

Park²

2014

BMB Reports

137

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“…Additionally, the 1,2-GDN/1,3 GDN ratio at 5 h of incubation was found to be 0.2 ± 0.02, indicating that NTG degradation was more mediated by chemical degradation [3] than by metabolic activation [1,4]. Thus, although this cell line has been used as a model to study vascular function, e.g., response to angiotensin stimulation [15], its utility for studying NTG metabolism may be somewhat limited. It should be noted however that, in these studies, the culture medium contained 0.002% each of ethanol and propylene glycol, which might inhibit the activities of cellular degradation enzymes.…”

Section: Resultsmentioning

confidence: 97%

Simultaneous determination of nitroglycerin and dinitrate metabolites in metabolism studies using liquid chromatography–mass spectrometry with electrospray ionization

Miyayama

Tsou

Fung

et al. 2006

Journal of Chromatography B

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“…Lectin‐like oxidized low density lipoprotein receptor‐1 (LOX‐1) is the main receptor for ox‐LDL on endothelial cells. The expression of LOX‐1 was also observed in human VSMCs and smooth muscle cells after vascular injury [19,29]. Furthermore, LOX‐1 mediated ox‐LDL‐induced VSMCs proliferation and played a role in neointimal formation after vascular injury [29].…”

Section: Discussionmentioning

confidence: 99%

“…Limor et al. [19] discovered that Ang II induced LOX‐1 expression in human VSMCs via a lipoxygenase (LOX)‐dependent pathway. Hsieh et al.…”

Section: Introductionmentioning

confidence: 99%

Ox‐LDL‐induced LOX‐1 expression in vascular smooth muscle cells: role of reactive oxygen species

Sun

Chen²

2010

Fundamemntal Clinical Pharma

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Oxidized low density lipoprotein (ox-LDL) and lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) have been implicated in the development of atherosclerosis. This study was designed to investigate the expression regulation of LOX-1 by ox-LDL and the potential underlying mechanisms in cultured rat vascular smooth muscle cells (VSMCs). VSMCs were treated with ox-LDL, and the expressions of LOX-1 mRNA and proteins were determined by RT-PCR and western blotting, respectively. The intracellular reactive oxygen species (ROS) production was monitored by flow cytometry with fluorescence probe, DCFH(2) -DA. The effect of several inhibitors including aspirin, NDGA, allopurinol, apocynin, and rotenone on ox-LDL-induced ROS formation and LOX-1 expression was also investigated. The roles of NF-κB p65 and JNK were explored. Ox-LDL significantly induced LOX-1 expression at both mRNA and protein levels in a dose-dependent and time-dependent manner. Aspirin, NDGA, and preconditioned apocynin suppressed ox-LDL-induced intracellular ROS production and LOX-1 expression, while allopurinol and rotenone failed to do so. Vitamin C and N-acetyl-l-cysteine demonstrated similar effect. Furthermore, both NF-κB p65 expression and phosphorylated JNK (p-JNK) to JNK expression ratio were elevated after ox-LDL treatment. In addition, the NF-κB inhibitor PDTC and JNK inhibitor SP600125 pretreatment partly abolished ox-LDL-induced LOX-1 expression. These findings suggested that ROS mediated ox-LDL-induced LOX-1 expression in VSMCs through NF-κB and JNK signaling pathways.

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Angiotensin II increases the expression of lectin-like oxidized low-density lipoprotein receptor-1 in human vascular smooth muscle cells via a lipoxygenase-dependent pathway

Cited by 23 publications

References 41 publications

Role of vascular smooth muscle cell in the inflammation of atherosclerosis

Role of vascular smooth muscle cell in the inflammation of atherosclerosis

Simultaneous determination of nitroglycerin and dinitrate metabolites in metabolism studies using liquid chromatography–mass spectrometry with electrospray ionization

Ox‐LDL‐induced LOX‐1 expression in vascular smooth muscle cells: role of reactive oxygen species

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