Paradoxical effects of cigarette smoke extract and high laminar flow on tumour necrosis factor-alpha induced VCAM-1 up-regulation – Implications for endothelial dysfunction

Teasdale, Jack E.; Hazell, Georgina; Newby, Andrew C.; White, Simon

doi:10.1016/j.atherosclerosis.2014.10.074

Cited by 6 publications

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“…19 Translational research completed by Teasdale et al (2014) and Pott et al (2017) also supported the findings that increased oxidative stress, reactive oxygene species, and VCAM-1 expression in endothelial cell cultures followed exposure to cigarette smoke. 20 Previously, researchers had been studying the influence of smoking on the levels of several biomarkers of oxidative stress, antioxidant status and redox status, including plasma hydroperoxides, e-NOS and VCAM-1. Using different assays to our study, they confirmed that smokers have elevated concentrations of VCAM-1 and compromised e-NOS status.…”

Section: Discussionmentioning

confidence: 99%

Acute effects of cigarette smoke on Endothelial Nitric Oxide synthase, vascular cell adhesion molecule 1 and aortic intima media thickness

et al. 2021

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Background. Cigarette smoking could induce endothelial dysfunction and the increase of circulating markers of inflammation by activation of monocytes. This can lead to increased intima media thickness (IMT) of entire blood vessels and result in acceleration of the atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. The aim of this study is to explore the link between cigarette smoking and its effect on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1). Methods. An experimental study with a post-test only controlled group design was used. We used 18 Wistar rats (Rattus norvegicus) randomly subdivided into two groups: group K (-) were not exposed to tobacco smoke, whereas group K (+) were exposed to smoke equivalent of more than 40 cigarettes for 28 days daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT. Results. Our results indicate that tobacco smoke can enhance the expression of VCAM-1 on rat cardiac vascular endothelial cells, resulting in a decreased expression of e-NOS level and increase of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT (r2 = 0.584, β = -0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT (r2 = 0.197, p = 0.065). Conclusion. Low e-NOS level and high VCAM-1 level observed after cigarette smoke exposure which may increase aortic IMT.

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Section: Discussionmentioning

confidence: 99%

Acute effects of cigarette smoke on Endothelial Nitric Oxide synthase, vascular cell adhesion molecule 1 and aortic intima media thickness

et al. 2021

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Cigarette Smoke Modulates Inflammation and Immunity via Reactive Oxygen Species-Regulated Trained Immunity and Trained Tolerance Mechanisms

Saaoud

Shao

Cornwell

et al. 2023

Antioxidants & Redox Signaling

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Acute Effects of Cigarette on Endothelial Nitric Oxide Synthase, Vascular Cell Adhesion Molecule 1 and Aortic Intima Media Thickness “Cigarette smoke–induced pro-atherogenic changes”

Ardiana

Santoso

Hermawan

et al. 2021

Preprint

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BackgroundCigarette smoking could induce endothelial dysfunction and increase of circulating markers of inflammation by activation of monocytes. This can lead to the increased of intima media thickness (IMT) of entire blood vessel and result acceleration of atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process.ObjectiveThe aim of this study is to explore the link between cigarette smoking on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1).MethodsAn experimental study with post-test only controlled group design was used in this study. We used 18 Wistar rats (Rattus norvegicus) randomly subdivided into 2 groups, group K (−) were given no tobacco smoking exposed, whereas group K (+) were exposed to 40 cigarettes smokes daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT.ResultsOur results indicate that tobacco smoke can enhance the expression of VCAM-1 on mouse cardiac vascular endothelial cell, resulting in decreased expression of e-NOS level and increased of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT (r2 = 0.584, β = −0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT (r2 = 0.197, p = 0.065).ConclusionLow e-NOS level and high VCAM-1 level observed following after cigarette smoke exposure may increase aortic IMT.Clinical significanceIncreasing evidence suggests that cigarette smoke exposure could induce VCAM-1 (enhance pro-atherogenic property),and decreased of e-NOS level (anti-atherogenic depletion). Thus, cigarette smoke may represent a significant risk factor for atherosclerosis by increasing aortic IMT. This evidence is discussed herein.

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Paradoxical effects of cigarette smoke extract and high laminar flow on tumour necrosis factor-alpha induced VCAM-1 up-regulation – Implications for endothelial dysfunction

Cited by 6 publications

References 0 publications

Acute effects of cigarette smoke on Endothelial Nitric Oxide synthase, vascular cell adhesion molecule 1 and aortic intima media thickness

Acute effects of cigarette smoke on Endothelial Nitric Oxide synthase, vascular cell adhesion molecule 1 and aortic intima media thickness

Cigarette Smoke Modulates Inflammation and Immunity via Reactive Oxygen Species-Regulated Trained Immunity and Trained Tolerance Mechanisms

Acute Effects of Cigarette on Endothelial Nitric Oxide Synthase, Vascular Cell Adhesion Molecule 1 and Aortic Intima Media Thickness “Cigarette smoke–induced pro-atherogenic changes”

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