Von Willebrand Factor, Hyperlipidaemia, and Vascular Disease

Blann, AD; Duffy, Aisling; Jp, Miller; McCollum, CN

doi:10.1042/cs082016pa

Cited by 5 publications

(8 citation statements)

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“…Furthermore, in this study, the vasoconstriction caused by ET-1 correlated inversely with plasma ET-1 concentrations, thus suggesting a reduced responsiveness to exogenous ET-1 that possibly reflected overactivity of the ET-1 system and ET-1 type A receptor downregulation. Interestingly, these authors also found normal baseline plasma levels of von Willebrand factor, a well-recognized marker of endothelial dysfunction, 27,36 further supporting the lack of endothelial alterations in patients with cardiac syndrome X.…”

Section: Discussionmentioning

confidence: 75%

Endothelial Activation in Patients With Cardiac Syndrome X

et al. 2000

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Section: Discussionmentioning

confidence: 75%

Endothelial Activation in Patients With Cardiac Syndrome X

et al. 2000

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“…In particular, ET-1 is elevated in plasma from atherosclerotic patients, 4,7 while vWf mediates platelet adhesion to the endothelium and protects factor VIII against proteolysis. 10 With regard to adhesion molecules, E-selectin is not released by resting vascular endothelial cells 25 and regulates leukocyte adhesion to the endothelium. 26 Accordingly, increased S-E-selectin expression by endothelial cells and marked interaction with the natural ligand sialyl-Lewis x expressed by leukocytes infiltrating the vascular wall have been shown in human atheroma.…”

Section: Discussionmentioning

confidence: 99%

“…Urinary albumin excretion (UAE), a well-known marker of vascular damage, 8 is associated with high plasma levels of von Willebrand factor (vWf,) 9 a glycoprotein released by damaged vascular endothelial cells. 10 Since UAE is higher in salt-sensitive than salt-resistant hypertensives, 11 this abnormality further suggests that hypertension-related endothelial damage is more marked in salt-sensitive than salt-resistant individuals.…”

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confidence: 99%

Clustering of Endothelial Markers of Vascular Damage in Human Salt-Sensitive Hypertension

et al. 1998

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Abstract-The contributing role of vascular endothelium in the development of hypertension-related vascular damage is well accepted. Salt-sensitive hypertension is characterized by a cluster of renal, hormonal, and metabolic derangements that might favor the development of cardiovascular and renal damage. To evaluate endothelial involvement in salt-sensitive essential hypertension, plasma levels of several markers of endothelial damage such as endothelin-1 (ET-1), von Willebrand factor (vWf), and soluble (S-) adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and 24-hour urinary albumin excretion (UAE) were measured in 39 nondiabetic, nonobese, never-treated essential hypertensive patients after intermediate (120 mmol/d), high (220 mmol/d), and low (20 mmol/d) NaCl diets. Patients were classified as salt sensitive (nϭ18) or salt resistant (nϭ21) according to their blood pressure responses to changes in dietary NaCl intake. Salt-sensitive hypertensives showed higher plasma ET-1 (PϽ0.05), vWf (PϽ0.005), and S-E-selectin levels (PϽ0.04) and increased UAE (PϽ0.05) than salt-resistant hypertensives. By contrast, circulating S-ICAM-1 and S-VCAM-1 concentrations were not significantly higher in salt-sensitive (596.56Ϯ177.05 ng/mL and 541.06Ϯ157.84 ng/mL, respectively) than salt-resistant patients (516.86Ϯ147.99 ng/mL and 449.48Ϯ158.91 ng/mL, respectively). During the intermediate NaCl diet, plasma ET-1 responses to oral glucose load were greater in salt-sensitive (PϽ0.05) than in salt-resistant patients. A marked (PϽ0.05) hyperinsulinemic response to oral glucose load was evident in salt-sensitive but not salt-resistant patients after each diet. This study shows increased plasma levels of the endothelium-derived substances E-selectin, vWf, and ET-1 in salt-sensitive hypertensives. Our findings support the hypothesis that salt sensitivity is correlated with an increased risk for developing hypertension-related cardiovascular damage. (Hypertension. 1998;32:862-868.)Key Words: endothelium Ⅲ cell adhesion molecules Ⅲ vasorelaxation Ⅲ sodium Ⅲ blood pressure S alt-sensitive hypertension is characterized by a cluster of renal, hormonal, and metabolic derangements that might favor the development of cardiovascular and renal complications.1,2 In this regard, the vascular endothelium modulates platelet aggregation, adhesion molecule expression, and vascular smooth muscle cell replication, 3 all of which contribute to atherogenesis. Interestingly, salt-sensitive hypertension is characterized by impaired endothelium-dependent vasorelaxation. 4 Furthermore, circulating levels of the endotheliumderived peptide endothelin-1 (ET-1) are higher, 5 while urinary ET-1 excretion is lower 6 and more responsive to salt loading 7 in salt-sensitive than salt-resistant patients. Urinary albumin excretion (UAE), a well-known marker of vascular damage, 8 is associated with high plasma levels of von Willebrand factor (vWf,) 9 a glycoprotein released by damaged vascular endotheli...

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“…Von Willebrand factor is also a regulator of the response to endothelial cell damage, platelet activation, and platelet plug formation at the site of injury. 60 , 61 , 62 , 63 C. v. viridis venom in southern Colorado contains high levels of snake venom metalloproteases (SVMPs; Smith et al., in review), which are known to attack microvessel structure by proteolytically degrading the basement membrane and disrupting endothelial cell adhesion leading to vessel damage and fluid extravasation. 64 , 65 , 66 This ultimately can result in local and systemic bleeding, tissue destruction, and ischemia.…”

Section: Discussionmentioning

confidence: 99%

Feasibility of detecting snake envenomation biomarkers from dried blood spots

Smith

Brandehoff

Pepin

et al. 2023

Analytical Science Advances

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Biofluid proteomics is a sensitive and high throughput technique that provides vast amounts of molecular data for biomarker discovery. More recently, dried blood spots (DBS) have gained traction as a stable, noninvasive, and relatively cheap source of proteomic data for biomarker identification in disease and injury. Snake envenomation is responsible for significant morbidity and mortality worldwide; however, much remains unknown about the systemic molecular response to envenomation and acquiring biological samples for analysis is a major hurdle. In this study, we utilized DBS acquired from a case of lethal rattlesnake envenomation to determine the feasibility of discovering biomarkers associated with human envenomation. We identified proteins that were either unique or upregulated in envenomated blood compared to non‐envenomated blood and evaluated if physiological response pathways and protein markers that correspond to the observed syndromes triggered by envenomation could be detected. We demonstrate that DBS provide useful proteomic information on the systemic processes that resulted from envenomation in this case and find evidence for a massive and systemic inflammatory cascade, combined with coagulation dysregulation, complement system activation, hypoxia response activation, and apoptosis. We also detected potential markers indicative of lethal anaphylaxis, cardiac arrest, and brain death. Ultimately, DBS proteomics has the potential to provide stable and sensitive molecular data on envenomation syndromes and response pathways, which is particularly relevant in low‐resource areas which may lack the materials for biofluid processing and storage.

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Von Willebrand Factor, Hyperlipidaemia, and Vascular Disease

Cited by 5 publications

References 0 publications

Endothelial Activation in Patients With Cardiac Syndrome X

Endothelial Activation in Patients With Cardiac Syndrome X

Clustering of Endothelial Markers of Vascular Damage in Human Salt-Sensitive Hypertension

Feasibility of detecting snake envenomation biomarkers from dried blood spots

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