Increased interleukin-8 expression by cigarette smoke extract in endothelial cells

Wang, Hongying; Ye, Yi-Ni; Zhu, Min; Cho, Chi-Hin

doi:10.1016/s1382-6689(00)00056-9

Cited by 31 publications

(23 citation statements)

References 18 publications

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“…Recently, both an increase and a decrease of eNOS mRNA and protein have been reported in relation to the effect of cigarette smoke in various experimental models. CS has been shown to inhibit pulmonary artery eNOS (31) and to suppress eNOS by ϳ52% in cultured endothelial cells (35). Conversely, Barua et al (2) found a higher eNOS expression in human umbilical vein endothelial cells treated with serum from smokers.…”

Section: No Production and Enos Protein Expressionmentioning

confidence: 98%

Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries

Guo¹,

Oldham²,

Kleinman³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Cigarette smoking (CS) is a major risk factor for vascular disease. The aim of this study was to quantitatively assess the influence of CS on mouse arteries. We studied the effect of short-term (6 wk) and long-term (16 wk) CS exposure on structural and mechanical properties of coronary arteries compared with that of control mice. We also examined the reversibility of the deleterious effects of CS on structural [e.g., wall thickness (WT)], mechanical (e.g., stiffness), and biochemical [e.g., nitric oxide (NO) by-products] properties with the cessation of CS. The left and right coronary arteries were cannulated in situ and mechanically distended. The stress, strain, elastic modulus, and WT of coronary arteries were determined. Western blot analysis was used to analyze endothelial NO synthase (eNOS) in the femoral and carotid arteries of the same mice, and NO by-products were determined by measuring the levels of nitrite. Our results show that the mean arterial pressure was increased by CS. Furthermore, CS significantly increased the elastic modulus, decreased stress and strain, and increased the WT and WT-to-radius ratio compared with those of control mice. The reduction of eNOS protein expression was found only after long-term CS exposure. Moreover, the NO metabolite was markedly decreased in CS mice after short- and long-term exposure of CS. These findings suggest that 16 wk of CS exposure can cause an irreversible deterioration of structural and elastic properties of mouse coronary arteries. The decrease in endothelium-derived NO in CS mice was seen to significantly correlate with the remodeling of arterial wall.

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Section: No Production and Enos Protein Expressionmentioning

confidence: 98%

Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries

Guo¹,

Oldham²,

Kleinman³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…These effects were abolished by recombinant SOD treatment suggesting cigarette smoke-mediated peroxidation/oxidative stress which regulates the molecular events in lung inflammation [190]. Similarly, several investigators have shown that cigarette smoke induces IL-8 release from human bronchial and alveolar epithelial and endothelial cells which may contribute to airway inflammation in smokers [191][192][193]. The increased IL-8 was significantly correlated with neutrophil counts in bronchial samples of BALF.…”

Section: Map Kinase Nf-κb and Ap-1 Activationmentioning

confidence: 99%

Oxidative Stress and Gene Transcription in Asthma and Chronic Obstructive Pulmonary Disease: Antioxidant Therapeutic Targets

Rahman¹

2002

CDTIA

102

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Inflammatory lung diseases such as asthma and Chronic Obstructive Pulmonary Disease (COPD) are characterised by systemic and local chronic inflammation and oxidative stress. The sources of the increased oxidative stress in patients with asthma and COPD derive from the increased burden of inhaled oxidants, and from the increased amounts of reactive oxygen species (ROS) generated by several inflammatory, immune and structural cells of the airways. Increased levels of ROS produced in the airways are reflected by increased markers of oxidative stress in the airspaces, sputum, breath, lungs and blood in patients with asthma and COPD. ROS, either directly or via the formation of lipid peroxidation products such as acrolein, 4-hydroxy-2-nonenal and F 2 -isoprostanes, may play a role in enhancing the inflammation through the activation of stress kinases (JNK, MAPK, p38, phosphoinositide 3 (PI-3)-kinase/PI-3K-activated serine-threonine kinase Akt) and redox sensitive transcription factors such as NF-κB and AP-1. Recent data have also indicated that oxidative stress and pro-inflammatory mediators can alter nuclear histone acetylation/deacetylation allowing access for transcription factor DNA binding leading to enhanced pro-inflammatory gene expression in various lung cells. Furthermore, oxidative stress may alter the balance between gene expression of pro-inflammatory mediators and antioxidant enzymes in favor of inflammatory mediators in the lung. Thus, the presence of oxidative stress may have important consequences for the pathogenesis of asthma and COPD. Identification of genes that predispose to the development of asthma and COPD may identify novel therapeutic targets. Future work is directed to understand the molecular mechanisms of antioxidants on ROS-mediated cell signaling pathways and inhibition of inflammatory response that would provide information for the development of novel antioxidant therapeutic targets in asthma and COPD. Effective wide spectrum antioxidant therapy that has good bioavailability and potency is urgently needed to control the localised oxidative and inflammatory processes that occur in the pathogenesis of asthma and COPD. In addition, development of such novel antioxidant compounds would be therapeutically useful in monitoring the oxidative and inflammatory biomarkers in the progression/severity of asthma and COPD.

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“…1 As such, cigarette smoke has been reported to induce many cellular effects, including DNA damage and apoptosis, activate protein kinase C, and inducing of interleukin-8 expression. 9,10 In the present study, we aimed to evaluate the cellular and molecular mechanism(s) by which cigarette smoke alters endothelial function. Specifically, we investigated the effects of cigarette smoke extract (CSE) on the major pathways of arginine and NO metabolism in endothelial cells using a series of complementary approaches.…”

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confidence: 99%

Adverse Effects of Cigarette Smoke on NO Bioavailability

et al. 2006

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Abstract-Endothelial dysfunction is a hallmark of cardiovascular disease, and the L-arginine:NO pathway plays a critical role in determining endothelial function. Recent studies suggest that smoking, a well-recognized risk factor for vascular disease, may interfere with L-arginine and NO metabolism; however, this remains poorly characterized. Accordingly, we performed a series of complementary in vivo and in vitro studies to elucidate the mechanism by which cigarette smoke adversely affects endothelial function. In current smokers, plasma levels of asymmetrical dimethyl-arginine (ADMA) were 80% higher (Pϭ0.01) than nonsmokers, whereas citrulline (17%; PϽ0.05) and N-hydroxy-L-arginine (34%; PϽ0.05) were significantly lower. Exposure to 10% cigarette smoke extract (CSE) significantly affected endothelial arginine metabolism with reductions in the intracellular content of citrulline (81%), N-hydroxy-L-arginine (57%), and arginine (23%), while increasing ADMA (129%). CSE significantly inhibited (38%) arginine uptake in conjunction with a 34% reduction in expression of the arginine transporter, CAT1. In conjunction with these studies, CSE significantly reduced the activity of eNOS and NO production by endothelial cells, while stimulating the production of reactive oxygen species. In conclusion, cigarette smoke adversely affects the endothelial L-arginine NO synthase pathway, resulting in reducing NO production and elevated oxidative stress. In conjunction, exposure to cigarette smoke increases ADMA concentration, the latter being a risk factor for cardiovascular disease. Key Words: smoking Ⅲ endothelium Ⅲ metabolism A therosclerotic coronary and cerebrovascular disease are leading causes of death and disability in the Western world, and cigarette smoking has been clearly identified as a risk factor for coronary artery disease (reviewed by Ambrose and Barua 1 ). In this context, measures of endothelial function have been associated with cardiovascular outcome, 2 and smoking has been widely associated with reduced endothelial function. 3 The endothelium plays a central role in the modulation of vascular tone, the inhibition of platelet aggregation and vascular smooth muscle proliferation, and a key participation in angiogenesis under appropriate conditions. NO is well recognized as playing a pivotal part in these endothelial properties, being produced by the endothelial isoform of NO from its preferred substrate L-arginine. In this context, provision of sufficient L-arginine is critical for the sustained production of NO supply, 4 mediated in endothelial cells (ECs) principally by the type 1 cationic amino acid transporter (CAT1). Previous studies indicate that deleterious actions of cigarette smoke on endothelial function could be mitigated by supplemental L-arginine; 5 however, to date, the precise basis for this interaction remains unclear. One explanation is that cigarette smoke exerts an inhibitory effect on components of the L-arginine:NO pathway to influence NO production. In addition, potential effects of cigar...

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Increased interleukin-8 expression by cigarette smoke extract in endothelial cells

Cited by 31 publications

References 18 publications

Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries

Effect of cigarette smoking on nitric oxide, structural, and mechanical properties of mouse arteries

Oxidative Stress and Gene Transcription in Asthma and Chronic Obstructive Pulmonary Disease: Antioxidant Therapeutic Targets

Adverse Effects of Cigarette Smoke on NO Bioavailability

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