Platelet reactivity, fibrinogen and smoking

Dotevall, Annika; Kutti, Jack; Teger‐Nilsson, Ann‐Catrine; Wadenvik, Hans; Wilhelmsen, Lars

doi:10.1111/j.1600-0609.1987.tb01424.x

Cited by 43 publications

(10 citation statements)

References 28 publications

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“…Cigarette smoking has also been shown to increase the circulating levels of fibrinogen and smokers have a higher risk for cardiovascular disease and thrombotic events (31,32). Oxidative stress has been considered as one of the mechanisms responsible for the development and progression of cardiovascular and pulmonary disorders and is increased, as reflected by indices of lipid peroxidation, in otherwise apparently healthy smokers (33,34).…”

Section: Discussionmentioning

confidence: 99%

Fibrinogen β-Chain Tyrosine Nitration Is a Prothrombotic Risk Factor

Parastatidis

Thomson

Burke

et al. 2008

Journal of Biological Chemistry

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Elevated levels of circulating fibrinogen are associated with an increased risk of atherothrombotic diseases although a causative correlation between high levels of fibrinogen and cardiovascular complications has not been established. We hypothesized that a potential mechanism for an increased prothrombotic state is the post-translational modification of fibrinogen by tyrosine nitration. Mass spectrometry identified tyrosine residues 292 and 422 at the carboxyl terminus of the ␤-chain as the principal sites of fibrinogen nitration in vivo. Immunoelectron microscopy confirmed the incorporation of nitrated fibrinogen molecules in fibrin fibers. The nitration of fibrinogen in vivo resulted in four distinct functional consequences: increased initial velocity of fibrin clot formation, altered fibrin clot architecture, increased fibrin clot stiffness, and reduced rate of clot lysis. The rate of fibrin clot formation and clot architecture was restored upon depletion of the tyrosine-nitrated fibrinogen molecules. An enhanced response to the knob "B" mimetic peptides Gly-His-Arg-Pro am and Ala-His-Arg-Pro am suggests that incorporation of nitrated fibrinogen molecules accelerates fibrin lateral aggregation. The data provide a novel biochemical risk factor that could explain epidemiological associations of oxidative stress and inflammation with thrombotic complications.Activation of the coagulation cascade converts soluble fibrinogen to insoluble fibrin, which polymerizes to produce, along with platelets, the hemostatic clot (1, 2). Whereas the normal activation of the coagulation cascade is essential for life, inappropriate activation may result in thrombosis and complications that arise from the formation of fibrin clots. Indeed pathologically induced thrombogenesis is associated with adverse cardiovascular events (3, 4), thromboembolism in chronic obstructive pulmonary disease (5), and vascular complications in autoimmune diseases (6). Because fibrinogen is an acute phase reactant, epidemiological studies have documented elevated fibrinogen levels in subjects with these disorders (7-10). Moreover, increased levels of circulating fibrinogen (11, 12) and common polymorphisms (13, 14) have been associated with an increased risk for thromboembolic episodes in subjects with coronary artery disease and in some cases of premature death from cardiovascular disease. Despite these established associations, a causative correlation between high levels of fibrinogen or polymorphisms and cardiovascular disease has not been firmly documented.Recently it was shown that the levels of proteins modified on tyrosine residues to form 3-nitrotyrosine, a protein marker of nitric oxide-derived reactive nitrogen species, are enhanced in the plasma of coronary artery disease patients and independently predict risk for coronary artery disease (15). Using affinity capture of fibrinogen followed by stable isotope, liquid chromatography (LC) 3 /tandem mass spectrometry (LC/MS/MS) quantification we reported increased levels of nitrated fibrinogen in...

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Section: Discussionmentioning

confidence: 99%

Fibrinogen β-Chain Tyrosine Nitration Is a Prothrombotic Risk Factor

Parastatidis

Thomson

Burke

et al. 2008

Journal of Biological Chemistry

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“…Toxic substances in tobacco are highly potent inflammatory stimuli and associated with tumorigenesis and clonal haematopoiesis (Hasselbalch, ). Smoking is associated with increased blood cells (Billimoria et al , ; Dotevall et al , ; Lowe et al , ; Parry et al , ; Smith et al , ; Wannamethee et al , ; Lao et al , ; Eisenga et al , ) (full list of references in Data S1) and MPN (Pasqualetti et al , ; Kroll et al , ; Leal et al , ; Lindholm Sorensen & Hasselbalch, ; Pedersen et al , ) in some but not all observational studies, likely due to differences in study size, effect size and direction, year published, sex and age distribution, geographical region, smoking status (current versus ex‐smoker), smoking duration, smoking intensity (heavy versus light) and ethnicity. Smoking and MPNs share several clinical and biochemical characteristics, including a high risk of thrombosis, partly explained by an elevated haematocrit and leukocytosis and in vivo leukocyte, platelet and endothelial activation (Hasselbalch, ).…”

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confidence: 99%

Smoking, blood cells and myeloproliferative neoplasms: meta‐analysis and Mendelian randomization of 2·3 million people

et al. 2019

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Meta-analyses and Mendelian randomization (MR) may clarify the associations of smoking, blood cells and myeloproliferative neoplasms (MPN). We investigated the association of smoking with blood cells in the Danish General Suburban Population Study (GESUS, n = 11 083), by meta-analyses (including GESUS) of 92 studies (n = 531 741) and MR of smoking variant CHRNA3 (rs1051730[A]) in UK Biobank, and with MPN in a meta-analysis of six studies (n (total/cases):1 425 529/2187), totalling 2 307 745 participants. In the meta-analysis the random-effects standardized mean difference (SMD) in current smokers versus non-smokers was 0Á82 (0Á75-0Á89, P = 2Á0 * 10 À108 ) for leukocytes, 0Á09 (À0Á02 to 0Á21, P = 0Á12) for erythrocytes, 0Á53 (0Á42-0Á64, P = 8Á0 * 10 À22 ) for haematocrit, 0Á42 (0Á34-0Á51, P = 7Á1 * 10 À21 ) for haemoglobin, 0Á19 (0Á08-0Á31, P = 1Á2 * 10 À3 ) for mean corpuscular haemoglobin (MCH), 0Á29 (0Á19-0Á39, P = 1Á6 * 10 À8 ) for mean corpuscular volume (MCV), and 0Á04 (À0Á04 to 0Á13, P = 0Á34) for platelets with trends for ever/ex-/current smokers, light/heavy smokers and female/male smokers. Analyses presented high heterogeneity but low publication bias. Per allele in CHRNA3, cigarettes per day in current smokers was associated with increased blood cell counts (leukocytes, neutrophils), MCH, red cell distribution width (RDW) and MCV. The pooled fixed-effects odds ratio for MPN was 1Á44 [95% confidence interval (CI): 1Á33-1Á56; P = 1Á8 * 10 À19 ; I 2 = 0%] in current smokers, 1Á29 (1Á15-1Á44; P = 8Á0 * 10 À6 ; I 2 = 0%) in ex-smokers, 1Á49 (1Á26-1Á77; P = 4Á4 * 10 À6 ; I 2 = 0%) in light smokers and 2Á04 (1Á74-2Á39, P = 2Á3 * 10 À18 ; I 2 = 51%) in heavy smokers compared with non-smokers.Smoking is observationally and genetically associated with increased leukocyte counts and red blood cell indices (MCH, MCV, RDW) and observationally with risk of MPN in current and ex-smokers versus non/neversmokers.

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“…In our study there was an increase in plasma fibrinogen and platelet count in smokers when compared to non smokers. In 2004, study conducted by Low AD et al concludes that smokers are more at risk of early development of thrombus which leads to impaired circulation [13][14][15] . Gs Tell et al suggested that there was increased platelet count in adolescent age group causing endothelial dysfunction and promotes vascular damage 16 .…”

Section: Discussionmentioning

confidence: 99%

Lipid Profile, Plasma Fibrinogen, and Platelet Count as Markers of Cardio Vascular Disease in Smokers Due to Free Radical Generation

Kannan¹,

Kumar²,

Ramaprabha³

et al. 2013

J Pharm Sci Innov

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Cigarette smoking & tobacco chewing are risk factors not only for oral and lung tumours but also for the development of systemic disorders like atherosclerosis, coronary artery disease and peripheral vascular disease. This study was undertaken to evaluate the lipid profile, plasma fibrinogen and platelet count in male smokers, compared with healthy non smokers in rural area of south India, Out of 100 male healthy volunteers, 50 members were healthy smokers and 50 healthy non smokers, subjects were divided in both groups in age around 30 to 45yrs, with no past history of diabetes mellitus, hypertension, hepatic disorders and were neither on anti hypertensive, lipid lowering drugs were included in the study. Lipid profile, plasma fibrinogen and platelet count were analyzed by standard methods. Our results showed mean platelet count for smokers is 2, 86,345per mm3 and for non-smokers 2, 04,484.6per mm3. The mean plasma fibrinogen concentration for smokers is 3.48gm/dl and for non smokers is 3.12gm/dl. The platelet count and plasma fibrinogen concentration shows a higher value for smokers when compared to non- smokers. This is statistically significant. The mean total cholesterol level for smokers (186±30.10) mg/dl and non smokers (166.3±24.26) mg/dl and the mean triglyceride level for smokers (175±59.43) mg/dl and non smokers (132.09±+33.80) mg/dl are also statistically significant. The mean HDL level for smokers (40.4±4.13) mg/dl and for non smokers (44.68±4.13) mg/dl, the mean LDL level for smokers (105.8±28.16) mg/dl and non smokers (89.68±16.50) mg/dl and the mean VLDL level for smokers (28.4± 8.16) mg/dl and non smokers (14.3.±3.2) mg/dl indicate that the Lipid profile also is statistically significant between the two groups. We concluded that there is an elevated lipid profile; plasma fibrinogen and platelet count in smokers when compared to non smokers, which shows that smokers have high risk of prevalence of cardiovascular and vessel wall diseases

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Platelet reactivity, fibrinogen and smoking

Cited by 43 publications

References 28 publications

Fibrinogen β-Chain Tyrosine Nitration Is a Prothrombotic Risk Factor

Fibrinogen β-Chain Tyrosine Nitration Is a Prothrombotic Risk Factor

Smoking, blood cells and myeloproliferative neoplasms: meta‐analysis and Mendelian randomization of 2·3 million people

Lipid Profile, Plasma Fibrinogen, and Platelet Count as Markers of Cardio Vascular Disease in Smokers Due to Free Radical Generation

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