scholarly journals 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”

2021 ◽  
Author(s):  
Meity Ardiana ◽  
Anwar Santoso ◽  
Hanestya O. Hermawan ◽  
Ricardo A. Nugraha ◽  
Budi S. Pikir ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Endothelial Nitric Oxide Synthase ◽  
Cell Adhesion Molecule ◽  
Intima Media Thickness ◽  
Cigarette Smoke Exposure ◽  
Vascular Cell Adhesion ◽  
Oxide Synthase ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Nitric Oxide

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.

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

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 396
Author(s):  
Meity Adriana ◽  
Anwar Santoso ◽  
Hanestya Okky Hermawan ◽  
Ricardo Adrian Nugraha ◽  
Budi Susetyo Pikir ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Tobacco Smoke ◽  
Endothelial Nitric Oxide Synthase ◽  
Cell Adhesion Molecule ◽  
Intima Media Thickness ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Oxide Synthase ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Nitric Oxide

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.

Soluble Vascular Cell Adhesion Molecule Levels, Endothelin-1 and Endothelial Nitric Oxide Synthase Gene Polymorphisms: Association with Clinical Symptoms in Sickle Cell Anemia.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2118-2118
Author(s):  
Wendell Vilas-Boas ◽  
Camylla Vilas Boas Figueiredo ◽  
Bruno A. V. Cerqueira ◽  
Thassila Pitanga ◽  
Angela Zanette ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gene Polymorphism ◽  
Adhesion Molecule ◽  
Endothelial Nitric Oxide Synthase ◽  
Cell Adhesion Molecule ◽  
Wild Type ◽  
Vascular Cell Adhesion ◽  
Soluble Adhesion Molecules ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Abstract Abstract 2118 Introduction: Vascular occlusions trigger most of the acute and chronic sickle cell anemia (HbSS) clinical complications and have been associated with high levels of soluble adhesion molecules and leukocytes activation. Accumulated evidence from clinical and experimental data shows that endothelin-1 (ET-1) plays an important role in the pathophysiology of the vascular system, because of its vasoconstrictor and hypertrophic activities. Endothelial nitric oxide synthase (eNOS) is an enzyme involved in nitric oxide (NO) synthesis pathway, a potent vasodilator and anti-inflammatory molecule. Polymorphisms in ET-1 and eNOS genes are associated with disturbance in ET-1 production and with reduced NO production respectively. The aim of this study was investigate the ET-1 5665G>T gene polymorphism and eNOS 786T>C gene promoter polymorphism with levels of soluble Intercellular Adhesion Molecule 1 (sICAM-1) and soluble Vascular Cell Adhesion Molecule 1 (sVCAM-1), biochemical markers and medical history of HbSS patients. Patients and Methods: We studied 51 HbSS patients from Northeast Brazil in attendance of the outpatient's clinic of the Foundation of Hematology and Hemotherapy of Bahia (HEMOBA). Biochemical analyses were measured by colorimetric methods, soluble adhesion molecules were measured by ELISA and the complete medical history was recorded by patient's record. The study was approved by the FIOCRUZ ethical committee and informed consents were signed by patients or official responsible.cerqueira Results: Our results showed genotype frequencies of 62.7% (32/51) of wild type (GG), 35.3% (18/51) of heterozygous (GT) and 2% (1/51) of homozygous (TT) for ET-1 5665G>T gene polymorphism. The eNOS 786T>C gene polymorphism showed 60.5% (23/38) of wild type, 34.2% (13/38) of heterozygous and 5.3% (2/38) homozygous. Both polymorphisms were in Hardy-Weinberg equilibrium. HbSS patients carriers of eNOS mutant allele (C) had the highest levels of sVCAM-1 (p= 0.015) (Fig. 1). Levels of sICAM were not related to any studied gene polymorphism. However, regarding to patients clinical history, we found a raised occurrence of acute chest syndrome (ACS) in carries of the ET-1 5665G>T mutant allele (Fig. 2). Discussion and Conclusion: Our study suggests that eNOS 786T>C and ET-1 5665G>T gene polymorphisms can participate of the HbSS pathophysiology. It is well known that high levels of circulating sVCAM are associating to an increased inflammatory state and VOC susceptibility, and our data show that eNOS variant in HbSS patients might be important to NO activity and anti-inflammatory vascular process. Also, the raised frequency of ACS, a major clinical feature in SCA which leads to patient mortality, was associated with the ET-1 variant showing the importance of the studied genes screening and their participation in these key molecules mechanism related to vascular health and VOC process. Disclosures: No relevant conflicts of interest to declare.

scholarly journals The Role of −786T/C Polymorphism in the Endothelial Nitric Oxide Synthase Gene in Males with Clinical and Biochemical Features of the Metabolic Syndrome

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Blazej Misiak ◽  
Marta Krolik ◽  
Anna Kukowka ◽  
Anna Lewera ◽  
Przemyslaw Leszczynski ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Syndrome ◽  
Nitric Oxide Synthase ◽  
Cigarette Smoking ◽  
Endothelial Nitric Oxide Synthase ◽  
International Diabetes Federation ◽  
The Metabolic Syndrome ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background. Extensive evidence, arising from models of endothelial nitric oxide synthase gene (NOS3)-knockout mice supports the role of endothelial malfunction in the pathogenesis of the metabolic syndrome (MS).Aims. The aim of this study was to evaluate the role of −786T/C polymorphism in the etiology of MS and assess previously reported interaction with cigarette smoking.Methods. Based on International Diabetes Federation 2005 criteria, we recruited randomly 152 subjects with MS and 75 subjects without MS.Results. Allelic and genotype frequencies did not differ significantly between both groups. Total cholesterol level (CHOLT) and intima-media thickness of carotid arteries were significantly higher in −786CC homozygotes, in comparison with −786TC and −786TT patients. Regarding current smoking status, −786C allele was associated with higher CHOLT than −786T allele.Conclusion. Our study indicates the putative role of −786T/C polymorphism in the development of hypercholesterolemia, in patients with MS, which might be enhanced by cigarette smoking.

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