Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Li, Ke; Yao, Wenqi; Zheng, Xinghua; Liao, Kan

doi:10.1038/cr.2009.76

Cited by 63 publications

(45 citation statements)

References 45 publications

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“…In endothelial cells and macrophages, both proinflammatory (e.g., priming of PKC, increase foam cell formation in macrophages) and anti-inflammatory pathways (e.g., increased eNOS phosphorylation and activation) are, in part, dependent on Akt/PKB activity. In one study, the plant alkaloid berberine was thought to increase atherosclerosis in ApoE null mice by supression of macrophage PTEN causing an increase in the expression of scavenger receptor SR-A, uptake of modified LDL, and foam cell formation (1027). Conversely, upregulation of PTEN in endothelial cells, either by specific alkaloids (810,1816) or by PPAR␥ agonists (810,838,909) substantially attenuated expression of the adhesion molecule VCAM-1 in response to the inflammatory cytokine TNF-␣ and decreased monocyte adherence while inhibiting endothelial proliferation and angiogenesis.…”

Section: Signaling Cassettes Activated By Rtk Are Mutually Supportivementioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

382

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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Section: Signaling Cassettes Activated By Rtk Are Mutually Supportivementioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

382

344

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“…In this study, we examined for the first time whether ox-LDL could regulate visfatin expression in RAW264.7 cells. Mouse RAW264.7 cells are a macrophage-like cell line and also can be induced to form foam cells by ox-LDL (Li et al 2009). Moreover, this cell line is more feasible for mechanistic studies compared with primary macrophages.…”

Section: Expression Of Visfatin In Plasma and Atherosclerotic Lesionsmentioning

confidence: 99%

“…Accumulating evidences have shown that some signaling pathway may be implicated in the uptake of ox-LDL by SR-A and CD36, including MAPK, PPAR, PI3K, and so on (Rahaman et al 2006;Xie et al 2011;Li et al 2009). CD36 was found to be mediated by Lyn and MEKK2 signaling pathway that were activated by ox-LDL specifically in macrophages.…”

mentioning

confidence: 99%

Visfatin induces cholesterol accumulation in macrophages through up-regulation of scavenger receptor-A and CD36

Zhou

Pan

Huang³

et al. 2013

Cell Stress and Chaperones

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As a new potential inflammatory mediator, visfatin plays an important role in inflammation and atherosclerosis. The formation of macrophage-derived foam cells occurs at the early stage of atherosclerosis and underlies the visible fatty streak. Recent studies have indicated that visfatin may be associated with the development of foam cells, but its exact effect and molecular mechanism remain unknown. This study aims to study the effect of visfatin on foamy cell formation and its underlying molecular mechanism. Visfatin levels were determined in apolipoprotein E (ApoE) knockout (KO) mice on a western diet for 16 weeks. Effects of visfatin in cholesterol accumulation were studied both in vivo and in vitro. The levels of scavenger receptors located in macrophage surface were measured in RAW264.7 cells after treatment with visfatin. Visfatin levels were much higher in ApoE KO mice than that in the control mice. Meanwhile, oxidized low-density lipoprotein induces both visfatin release from RAW264.7 cells and its cellular levels within 24 h. Visfatin promotes lipid accumulation mainly through excessive cholesterol uptake not only in RAW264.7 cells but also in peritoneal macrophages isolated from ApoE KO mice. Furthermore, visfatin induces the activation of scavenger receptors (SR)-A and cluster of differentiation (CD)36, but not that of SR-BI, ATP-binding cassette transporter (ABC)A1, or ABCG1 in RAW264.7 cells. Both transcriptional and posttranscriptional regulation may work in concert to mediate the expression of SR-A and CD36 in visfatin-treated cells. Visfatin induces cholesterol accumulation in macrophages and accelerates the process of atherosclerosis mainly through modulating the expression of SR-A and CD36.

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“…For instance, the pervasive effects of Tanshinone and Berberin in the prevention and cure of common cardiovascular diseases has been clarified [7,8]. In the current study, Aloeemodin (Fig.…”

Section: Introductionmentioning

confidence: 99%

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

Sun

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: High-fat diet (HFD) causes cardiac electrical remodeling and increases the risk of ventricular arrhythmias. Aloe-emodin (AE) is an anthraquinone component isolated from rhubarb and has a similar chemical structure with emodin. The protective effect of emodin against cardiac diseases has been reported in the literature. However, the cardioprotective property of AE is still unknown. The present study investigated the effect of AE on HFD-induced QT prolongation in rats. Methods: Adult male Wistar rats were randomly divided into three groups: control, HFD, and AE-treatment groups. Normal diet was given to rats in the control group, high-fat diet was given to rats in HFD and AE-treatment groups for a total of 10 weeks. First, HFD rats and AE-treatment rats were fed with high-fat diet for 4 weeks to establish the HFD model. Serum total cholesterol and triglyceride levels were measured to validate the HFD model. Afterward, AE-treatment rats were intragastrically administered with 100 mg/kg AE each day for 6 weeks. Electrocardiogram monitoring and whole-cell patch-clamp technique were applied to examine cardiac electrical activity, action potential and inward rectifier K + current (I K1 ), respectively. Neonatal rat ventricular myocytes (NRVMs) were subjected to cholesterol and/or AE. Protein expression of Kir2.1 was detected by Western blot and miR-1 level was examined by real-time PCR in vivo and in vitro, respectively. Results: In vivo, AE significantly shortened the QT interval, action potential duration at 90% repolarization (APD 90 ) and resting membrane potential (RMP), which were markedly elongated by HFD. AE increased I K1 current and Kir2.1 protein expression which were reduced in HFD rats. Furthermore, AE significantly inhibited pro-arrhythmic miR-1 in the hearts of HFD rats. In vitro, AE decreased miR-1 expression levels resulting in an increase of Kir2.1 protein levels in cholesterol-enriched NRVMs. Conclusions: AE prevents HFD-induced QT prolongation by repressing miR-1 and upregulating its target Kir2.1. These findings suggest a novel pharmacological role of AE in HFD-induced cardiac electrical remodeling.

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Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Cited by 63 publications

References 45 publications

Molecular Biology of Atherosclerosis

Molecular Biology of Atherosclerosis

Visfatin induces cholesterol accumulation in macrophages through up-regulation of scavenger receptor-A and CD36

Aloe-Emodin Relieves High-Fat Diet Induced QT Prolongation via MiR-1 Inhibition and IK1 Up-Regulation in Rats

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