3-Hydroxyanthranilic acid, one of l-tryptophan metabolites, inhibits monocyte chemoattractant protein-1 secretion and vascular cell adhesion molecule-1 expression via heme oxygenase-1 induction in human umbilical vein endothelial cells

Pae, Hyun‐Ock; Oh, Gi‐Su; Lee, Bok-Soo; Rim, Joung Sik; Kim, Young‐Myeong; Chung, Hun‐Taeg

doi:10.1016/j.atherosclerosis.2005.09.010

Cited by 73 publications

(54 citation statements)

References 38 publications

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“…NF-кB activation is a critical process for accelerating atherosclerosis and neo-intima hyperplasia (34). Pae et al found that the HO-1 inducer cobalt protoporphyrin can inhibit TNF-α-induced NF-кB activation in human umbilical vein endothelial cells and that the effect could be reversed by the HO-1 inhibitor tin protoporphyrin (35). Our present results also show that NF-кB activity and TNF-α levels were highest in the HFD + Z group and lowest in the HFD + H group, indicating the antiinflammatory effect of the HO-1 system.…”

Section: Discussionsupporting

confidence: 77%

Effects of Induction/Inhibition of Endogenous Heme Oxygenase-1 on Lipid Metabolism, Endothelial Function, and Atherosclerosis in Rabbits on a High Fat Diet

Liu¹,

Wu³

et al. 2012

J Pharmacol Sci

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Abstract. The heme oxygenase-1 (HO-1) / carbon monoxide (CO) system has been presumed as a therapeutic target for preventing atherosclerosis. However, the exact mechanism(s) underlying this system remains largely undefined. This study aims to examine the influence of induction/inhibition of HO-1 on atherosclerotic plaque using pharmacological approaches and to elucidate potential mechanisms. Rabbits were randomly assigned to receive a standard diet (control group), high fat diet (HFD), HFD plus HO inducer hemin (HFD + H group), and HFD plus an HO inhibitor, zinc protoporphyrin-9 (ZnPP9, HFD + Z group). Atherosclerotic plaque was evaluated using oil red O staining and histological analyses. Immunohistochemistry, western blotting, and RT-PCR were employed to study the expression of HO-1 and endothelin-1 (ET-1). Levels of CO, nitric oxide (NO), eNOS/iNOS activities, NF-κB activity, and TNF-α level were determined. No significant differences of serum lipid levels were observed among the HFD, HFD + Z, and HFD + H groups. In rabbits, HFD induced typical atherosclerotic plaque and increased intima/media thickness ratio, which was markedly reduced in the HFD + H group and further aggravated in the HFD + Z group. Furthermore, hemin increased HO-1 expression, CO levels, and eNOS activity, while decreasing iNOS levels, ET-1 expression, NF-κB activity, and TNF-α level. ZnPP9 caused opposite effects. Induction of the endogenous HO-1/CO system by hemin can prevent atherosclerosis though increasing CO levels, regulating eNOS activity, NF-κB activity, TNF-α levels, and ET-1 levels in rabbits. Our results add new evidence for the importance of HO-1 in the genesis and development of atherosclerosis and provide several possible mechanisms underlying the antiatherosclerosis effects of HO-1.

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Section: Discussionsupporting

confidence: 77%

Effects of Induction/Inhibition of Endogenous Heme Oxygenase-1 on Lipid Metabolism, Endothelial Function, and Atherosclerosis in Rabbits on a High Fat Diet

Liu¹,

Wu³

et al. 2012

J Pharmacol Sci

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“…6 -8 Bilirubin is an antioxidant under physiological conditions, inhibiting inflammation in the vasculature. 1,4 These properties appear to allow bilirubin to inhibit multiple steps in atherogenesis. It is worth noting that we did identify a strong inverse correlation between bilirubin and hsCRP (r = −0.117, P < 0.001), supporting the theory that bilirubin suppresses atherogenesis through inhibition of systemic inflammatory activity.…”

Section: Discussionmentioning

confidence: 99%

“…effects on vasculature. 4,5 Oxidative stress and inflammation are fundamental to the arteriopathy. 6 -8 Bilirubin was proven to act against plaque formation and subsequent atherosclerosis, 1 which was further confirmed by the studies revealing the relationships between bilirubin and peripheral artery disease (PAD) and carotid intima-media thickness (IMT).…”

Section: Introductionmentioning

confidence: 99%

Inverse Relation of Total Serum Bilirubin to Coronary Artery Calcification Score Detected by Multidetector Computed Tomography in Males

Zhang

Bian

Kim

et al. 2012

Clinical Cardiology

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Background:Serum total bilirubin has been suggested to have potential anti‐inflammatory and antioxidant effects on the vasculature, acting against plaque formation and subsequent atherosclerosis. This study was designed to assess the association of serum total bilirubin with coronary artery calcification (CAC).Hypothesis:Individuals with higher bilirubin level would be less likely to develop CAC.Methods:Male subjects (N = 3408) underwent evaluation of CAC by cardiac computed tomography. Correlation and logistic regression analysis were performed to assess the relationships between CAC score and other variables.Results:Subjects with a higher CAC score had significantly lower total bilirubin level (P = 0.001). Total bilirubin level was negatively correlated with CAC score (r = −0.052, P = 0.002). A 0.1‐mg/dL increase in bilirubin was associated with a reduced odds ratio (OR) of the risk by 29.2% for a CAC score above 100 (OR: 0.708, 95% confidence interval: 0.542‐0.927, P = 0.012) after adjustment for several variables. Bilirubin was inversely correlated with high‐sensitivity C‐reactive protein (hsCRP) (r = −0.117, P < 0.001).Conclusions:This study demonstrated an independent inverse association between serum total bilirubin and CAC score in males. Low serum bilirubin concentration would be useful as a potential risk factor for CAC in males. Additionally, reduced hsCRP may be 1 of the mechanisms for how bilirubin reduces CAC. © 2012 Wiley Periodicals, Inc.Additional Supporting Information may be found in the online version of this article.Zheng‐Yun Zhang, MD, and Lu‐Qin Bian, MD, contributed equally to this work.The authors have no funding, financial relationships, or conflicts of interest to disclose.

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“…Our finding the FIR therapy inhibits the expression of EC adhesion molecules and monocyte adhesion to endothelium via the HO-1-derived formation of bilirubin is consistent with studies demonstrating that overexpression of HO-1 or the exogenous application of bilirubin exerts an antiinflammatory effect by blocking the activation of the transcription factor NF-B, which is strictly required for cytokine-mediated induction of endothelial adhesion receptors. [33][34][35][36] The ability of FIR radiation to stimulate vascular HO-1 gene expression may contribute to its therapeutic effect in maintaining the patency of AVFs in HD patients. 10 Aside from its potent antiinflammatory action, HO-1 may also preserve blood flow through the AVF by inhibiting vascular smooth muscle cell (VSMC) proliferation, platelet aggregation, and vasospasm (see references [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

Far Infrared Therapy Inhibits Vascular Endothelial Inflammation via the Induction of Heme Oxygenase-1

Lin¹,

Liu

Peyton

et al. 2008

ATVB

116

115

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Objective-Survival of arteriovenous fistulas (AVFs) in hemodialysis patients is associated with both far infrared (FIR) therapy and length polymorphisms of the heme oxygenase-1 (HO-1) promoter. In this study, we evaluated whether there is an interaction between FIR radiation and HO-1 in regulating vascular inflammation. Methods and Results-Treatment of cultured human umbilical vein endothelial cells (ECs) with FIR radiation stimulated HO-1 protein, mRNA, and promoter activity. HO-1 induction was dependent on the activation of the antioxidant responsive element/NF-E2-related factor-2 complex, and was likely a consequence of heat stress. FIR radiation also inhibited tumor necrosis factor (TNF)-␣-mediated expression of E-selectin, vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-8, and the cytokine-mediated adhesion of monocytes to ECs. The antiinflammatory action of FIR was mimicked by bilirubin, and was reversed by the HO inhibitor, tin protoporphyrin-IX, or by the selective knockdown of HO-1. Finally, the antiinflammatory effect of FIR was also observed in patients undergoing hemodialysis. Key Words: endothelium Ⅲ far infrared therapy Ⅲ inflammation Ⅲ leukocyte adhesion A well-functioning vascular access is necessary for achieving adequate hemodialysis (HD) in patients with end stage renal failure. Approximately 17% to 25% of HD patient hospitalizations in the United States arise from vascular access complications, with an annual cost of more than 1 billion US dollars, which continues to grow. 1 Nearly 85% of vascular access failures arise from thromboses, more than 80% of which are associated with stenoses, 2 which usually presents with inadequate blood flow. 3,4 The causative factors of vascular access stenosis include small diameter of artery and vein, surgical technique, previous venipunctures, hemodynamic stress, and the presence of accessory veins. 5 Moreover, many factors leading to endothelial dysfunction, such as oxidative stress, hyperhomocysteinemia, platelet activation, and inflammation are associated with arteriovenous fistula (AVF) failure. 5 The histological features of vascular access stenosis comprise vascular inflammation, intimal hyperplasia, and excessive accumulation of extracellular matrix. 5 Despite these findings, the cause of stenoses remains unknown in a significant proportion of HD patients. This interindividual variation may relate to differences in the genetic background that may influence susceptibility to vascular inflammation and neointima formation after endothelial and smooth muscle injury. 6,7 Consistent with this notion, AVF survival was reported to be associated with specific genetic polymorphisms of transforming growth factor (TGF)-␤1 8 and methylene tetrahydrofolate reductase. 9 In addition, we recently identified a length polymorphism in the heme oxygenase-1 (HO-1) gene that is associated with patency of AVFs. 10 HO-1 catalyzes the oxidative degradation of heme into equimolar amounts of biliverdin,...

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3-Hydroxyanthranilic acid, one of l-tryptophan metabolites, inhibits monocyte chemoattractant protein-1 secretion and vascular cell adhesion molecule-1 expression via heme oxygenase-1 induction in human umbilical vein endothelial cells

Cited by 73 publications

References 38 publications

Effects of Induction/Inhibition of Endogenous Heme Oxygenase-1 on Lipid Metabolism, Endothelial Function, and Atherosclerosis in Rabbits on a High Fat Diet

Effects of Induction/Inhibition of Endogenous Heme Oxygenase-1 on Lipid Metabolism, Endothelial Function, and Atherosclerosis in Rabbits on a High Fat Diet

Inverse Relation of Total Serum Bilirubin to Coronary Artery Calcification Score Detected by Multidetector Computed Tomography in Males

Far Infrared Therapy Inhibits Vascular Endothelial Inflammation via the Induction of Heme Oxygenase-1

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