Lipopolysaccharide Down-regulates ABCA1 Expression in Foam Cells in a Nucleus Factor-κB Pathway-dependent Manner*

Cao, Dongli; Yin, Kai; Zhang, Mo; Hao, Xinrui; Hu, Yan‐Wei; Li, Xiaoxu; Tang, Yaling; Tang, Chao-Ke

doi:10.3724/sp.j.1206.2009.00738

Cited by 5 publications

(5 citation statements)

References 17 publications

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“…In the new hypercholesterolemia zebrafish model, knockdown of TLR4 can significantly reduce lipid accumulation in macrophages at the early stages of atherosclerotic plaque [ 30 ]. Additionally, LPS decreased ABCA1 expression in foam cells through the NF-κB-dependent pathway [ 31 ]. Besides, pro-inflammatory endothelial cells (ECs) dysfunction induced by LPS is associated with the deficiency of Intersectin-1s (ITSN-1s).…”

Section: Relationship Between Rct and Inflammatory Responsementioning

confidence: 99%

Caveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in Atherosclerosis

Qin

Zhu

et al. 2016

IJMS

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Lipid disorder and inflammation play critical roles in the development of atherosclerosis. Reverse cholesterol transport is a key event in lipid metabolism. Caveolae and caveolin-1 are in the center stage of cholesterol transportation and inflammation in macrophages. Here, we propose that reverse cholesterol transport and inflammation in atherosclerosis can be integrated by caveolae and caveolin-1.

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Section: Relationship Between Rct and Inflammatory Responsementioning

confidence: 99%

Caveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in Atherosclerosis

Qin

Zhu

et al. 2016

IJMS

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“…In the case of EBV infection, the expression of LMP1 inhibited the expression of SPLUNC1 in nasopharyngeal epithelial cells, leading to loss of innate immunity. In addition, SPLUNC1 may regulate miR141 [94] and the downstream PTEN-AKT signaling [113,114], and also the MAPK, NF-κB [115], Bcl-2/Bax [116], and toll-like receptor [109,117119] inflammatory response pathways [120], and ultimately the control of the cell cycle [121]. This pathway regulates the apoptotic cellular defense mechanism against cancer.…”

Section: Important Genes In Npc Carcinogenesismentioning

confidence: 99%

Nasopharyngeal carcinoma: Advances in genomics and molecular genetics

Zeng

Huang

Zhang

et al. 2011

Sci. China Life Sci.

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Nasopharyngeal carcinoma (NPC) is a squamous-cell carcinoma that arises in the epithelial lining of the nasopharynx [1]. This neoplasm has a notable ethnic and geographic distribution, being of high prevalence in southern China but rare in other parts of the world [2]. Familial clustering of NPC has been observed in diverse populations [3]. Elevated levels of circulating free Epstein-Barr virus (EBV) DNA and EBV-related antibodies in sera, as well as EBV DNA in tumor cells, have been consistently detected in individuals with NPC [4,5]. These studies have revealed that the risk factors of NPC are both environmental and genetic. How the risk factors interact, and the genes that are involved in the development of NPC, are not well understood [6].

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“…Liu and colleagues [6] (South Central University) investigated the effect of paraoxon, an active metabolite of organophosphorus insecticide that increases cholesterol retention in macrophages [4], on ABCA1 expression and ABCA1-dependent cholesterol efflux in RAW 264.7 macrophage-derived foam cells, and found that paraoxon significantly downregulated ABCA1 expression and reduced ABCA1-dependent cholesterol efflux through cyclic AMP signaling pathway. Our group [7,8] (University of South China) found that LPS and interferon (IFN)-γ can downregulate expression of ABCA1 and promote accumulation of lipid and decrease cellular cholesterol efflux in THP-1 macrophage-derived foam cells.Vascular endothelial dysfunction is known as the primary step in vascular inflammation and atherogenesis. Liu and colleagues [9] (Peking Union Medical College and Chinese Academy of Medical Sciences) discovered that human paraoxonase gene cluster transgenic overexpression represses atherogenesis and promotes atherosclerotic plaque stability in apoE-null mice.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Inflammation, lipid metabolism dysfunction, and hypertension: Active research fields in atherosclerosis-related cardiovascular disease in China

Yin

Tang

2011

Sci. China Life Sci.

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Atherosclerosis-related cardiovascular disease is one of the leading causes of death in China [1]. With advances in our understanding of the molecular mechanisms of atherosclerosis vascular inflammation, lipid metabolism dysfunction, and hypertension are regarded as the main pathogenetic pathways of both early atherogenesis and advanced plaque rupture [2,3]. Currently, much attention is being paid to the control of these pathways, which offers the potential for development of novel therapeutic approaches in the treatment of cardiovascular disease in China.In the past few decades, considerable evidence has underscored that atherosclerosis is a chronic inflammatory disease of the arterial wall, where numerous molecular inflammatory components such as organophosphate and lipopolysaccharide (LPS) play crucial roles in the development of atherosclerosis [4,5]. ATP-binding cassette transporter A1 (ABCA1), a cytomembrane transporter first cloned in 1994, has been identified as playing a key role in cholesterol reverse transport (RCT), which is regarded as anti-atherosclerotic. Evidence from many recent studies indicates that inflammation impairs RCT, and many atherogenic-related mediators play distinct regulatory roles in ABCA1 expression [2]. Liu and colleagues [6] (South Central University) investigated the effect of paraoxon, an active metabolite of organophosphorus insecticide that increases cholesterol retention in macrophages [4], on ABCA1 expression and ABCA1-dependent cholesterol efflux in RAW 264.7 macrophage-derived foam cells, and found that paraoxon significantly downregulated ABCA1 expression and reduced ABCA1-dependent cholesterol efflux through cyclic AMP signaling pathway. Our group [7,8] (University of South China) found that LPS and interferon (IFN)-γ can downregulate expression of ABCA1 and promote accumulation of lipid and decrease cellular cholesterol efflux in THP-1 macrophage-derived foam cells.Vascular endothelial dysfunction is known as the primary step in vascular inflammation and atherogenesis. Liu and colleagues [9] (Peking Union Medical College and Chinese Academy of Medical Sciences) discovered that human paraoxonase gene cluster transgenic overexpression represses atherogenesis and promotes atherosclerotic plaque stability in apoE-null mice. They also found that endothelium-specific overexpression of class III deacetylase SIRT1 decreases atherosclerosis in apoE-deficient mice [10]. Liu et al. [11] (Central South University) found that treatment with paraoxon resulted in significant inhibition of endothelium-dependent relaxation (EDR) in rabbits as well as a significant decrease of endothelial nitric oxide synthase (eNOS) activity in isolated aorta. These findings suggest that subchronic exposure to environmentally relevant matter such as LPS and organophosphate, even at low concentrations, potentiates inflammation, cholesterol retention, and

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Lipopolysaccharide Down-regulates ABCA1 Expression in Foam Cells in a Nucleus Factor-κB Pathway-dependent Manner*

Cited by 5 publications

References 17 publications

Caveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in Atherosclerosis

Caveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in Atherosclerosis

Nasopharyngeal carcinoma: Advances in genomics and molecular genetics

Inflammation, lipid metabolism dysfunction, and hypertension: Active research fields in atherosclerosis-related cardiovascular disease in China

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