Plasma Levels of Inflammatory Biomarkers in Peripheral Arterial Disease

Signorelli, Salvatore Santo; Anzaldi, Massimiliano; Libra, Massimo; Navolanic, Patrick M.; Malaponte, Graziella; Mangano, Katia; Quattrocchi, Cinzia; Marco, Roberto Di; Fiore, Valerio; Neri, Sergio

doi:10.1177/0003319716633339

Cited by 43 publications

(53 citation statements)

References 48 publications

(54 reference statements)

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“…Interleukin-6 blood levels correlate with dysfunction of the endothelial cells, arterial stiffness, and predict risk of vascular events [17,18]. Decreasing the IL-6 level in patients with PAD seems to be a desirable effect, preventing progression of the disease [19]. Previously, we found that sulodexide also inhibits IL-6 release from human venous endothelial cells [9].…”

Section: Discussionmentioning

confidence: 96%

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

Sosińska

Baum²,

Maćkowiak³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Dysfunction of the arterial endothelial cells promotes the progression of atherosclerosis. We studied how exposure of human arterial endothelial cells to atherosclerotic serum from patients with peripheral artery disease changes the secretory activity of these cells, and whether that reaction is modified by sulodexide. Methods: Endothelial cells in in vitro culture were exposed to standard culture medium ± 100pg/mL Interleukin-1(IL-1) or to medium supplemented with 20% atherosclerotic serum. Afterwards, the expression of genes responsible for the synthesis of Interleukin-6 (IL-6), Vascular Cell Adhesion Protein-1 (VCAM-1) and Von Willebrand Factor (VWF) was evaluated, together with the secretion of these compounds. Additionally, the effect of sulodexide on these processes was studied. Results: Atherosclerotic serum stimulated the expression of IL6, VCAM-1 and VWF genes in endothelial cells, which was followed by increased secretion of these compounds by 179%, 121% and 116%, respectively. Sulodexide (0.5 LRU/mL) reduced atherosclerotic serum-induced increased expression of genes for IL-6 (-32%), VCAM-1 (-20%) and VWF (-42%), and lowered secretion of these molecules: IL-6 (-27%), VCAM-1(-27%), VWF (-25%). Sulodexide also reduced, in a dose- dependent manner, secretion of IL6 from unstimulated and stimulated with IL-1 endothelial cells. Conclusions: Atherosclerotic serum induces proinflammatory and prothrombotic phenotype in arterial endothelium, which is partially reduced by sulodexide, via inhibition of genes expression, and in consequence lower secretory activity.

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Section: Discussionmentioning

confidence: 96%

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

Sosińska

Baum²,

Maćkowiak³

et al. 2016

Cell Physiol Biochem

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“…Several potential inflammatory biomarkers for the prediction of atherosclerosis have been proposed including CRP, IL-6, TNF-α, SELL, SELP, VCAM-1, ICAM-1 [39][40][41]. CRP is the most promising inflammatory biomarker predicting future cardiovascular events [42].…”

Section: Discussion/conclusionmentioning

confidence: 99%

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

et al. 2018

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Background: L-carnitine can be metabolized to trimethylamine N-oxide (TMAO), a molecule that promotes atherogenesis through its interaction with macrophages and lipid metabolism. Objective: The aim of the present study was to assess whether L-carnitine supplementation may promote changes in selected serum biomarkers of atherosclerosis. Methods: Before the start, in the mid-point and after completing the 24-weeks supplementation protocol, fasting blood samples were taken from the antecubital vein. Plasma free L-carnitine and TMAO were determined by the UPLC/MS/MS method. Serum proteins were determined by the enzyme immunoassay method using commercially available kits. Total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and triglycerides have been determined using standard automatic analyzer. Results: L-carnitine supplementation elevated fasting plasma carnitine in the mid-point of our study and it remained increased until the end of supplementation period. Moreover, it induced tenfold increase in plasma TMAO concentration but did not affect serum C-reactive protein, interleukin-6, tumour necrosis factor-α, L-selectin, P-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 or lipid profile markers. Conclusion: We demonstrated that although oral L-carnitine supplementation significantly increased plasma TMAO concentration, no lipid profile changes or other markers of adverse cardiovascular events were detected in healthy aged women over the period of 24 weeks.

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“…1 They reported that higher plasma levels of inflammatory biomarkers were related to the development of peripheral arterial disease (PAD). 1 The cause of PAD is usually atherosclerosis.…”

mentioning

confidence: 99%

“…1 Perhaps, some of the basic and cheaper methods like C-reactive protein, neutrophil to lymphocyte ratio, and so on, could be analyzed 4 ; however, this comprehensive profile is better.…”

mentioning

confidence: 99%

Which Came First, the Chicken or the Egg? Paradox in Peripheral Arterial Diseases

et al. 2017

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Plasma Levels of Inflammatory Biomarkers in Peripheral Arterial Disease

Cited by 43 publications

References 48 publications

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

Which Came First, the Chicken or the Egg? Paradox in Peripheral Arterial Diseases

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