Compared with control, systemic administration of ADSCs-derived exosomes significantly increased the expression of von Willebrand factor (an endothelia cell marker) and doublecortin (a neuroblasts marker) and improved functional recovery in stroke rats.
The analysis found that high vWF levels were associated with increased risks of all-cause death (RR 1.56; 95% CI 1.16 to 2.11, p=0.00400), cardiovascular death (RR 1.91; 95% CI 1.20 to 3.03, p=0.00600), MACE (RR 1.83; 95% CI 1.28 to 2.62, p=0.00090), stroke (RR 1.69; 95% CI 1.08 to 2.64, p=0.02000) and bleeding (RR 2.01; 95% CI 1.65 to 2.45, p<0.00001) in patients with AF.
The VWF/ADAMTS-13 interaction has more recently emerged as a causative risk factor in the pathogenesis of pediatric stroke and secondary microangiopathies.
Therapeutic inhibition of VWF by novel agents appears particularly promising for secondary prevention of stroke recurrence in specific sub-groups of patients such as those suffering from large artery atherosclerosis, as designated according to the TOAST classification.
Our study suggests that increased vWF levels and presence of HMWMs could be related to cerebrovascular disease and may represent useful biomarkers for stroke in AF.
During the 2-month interval prior to an event, cases (n = 48) had higher levels of the vWF and ADAMTS13 than controls (n = 95; P = .05), but significance was lost after adjusting for the baseline differences in myocardial infarction, unstable angina, and stroke.
The results showed that combination treatment notably reduced neurological injury after stroke and increased the expression of astrocyte-derived vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), and von Willebrand factor-positive vascular density in the ischemic boundary zone as evaluated by immunofluorescence staining.
Previous studies in adults and mice have implicated ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13), also known as von Willebrand factor (VWF)-cleaving protease, as a protective factor for stroke.
Ring chromosome 12 with inverted microduplication of 12p13.3 involving the Von Willebrand Factor gene associated with cryptogenic stroke in a young adult male.
We report that deficiency or reduction of VWF reduces infarct volume up to 2-fold after focal cerebral ischemia in mice, thus showing the importance of VWF in stroke injury.
This finding suggests that high shear-induced platelet activation mediated by GP Ibalpha and von Willebrand factor is an important contributor to ATF in the stroke population.
C-reactive protein, ADAMTS13, and genetic variation did not affect the association between vWF and the relative risk of stroke, whereas blood group did affect the association.
Purported mechanisms for migraine-associated stroke include involvement of the vasculature (including vasospasm, arterial dissection and small vessel arteriopathy), hypercoagulability (elevated von Willebrand Factor, platelet activation) and elevated risk of cardioembolism (patent foramen ovale, atrial septal aneurysm).
Platelet glycoprotein IIb/IIa (GpIIb-IIIa), a membrane receptor for fibrinogen and von Willebrand factor, has been implicated in the pathogenesis of acute coronary syndromes but has not been previously investigated in relation to stroke in young adults.
Polymorphisms of the human platelet antigens HPA-1, HPA-2, HPA-3, and HPA-5 on the platelet receptors for fibrinogen (GPIIb/IIIa), von Willebrand factor (GPIb/IX), and collagen (GPIa/IIa) are not correlated with an increased risk for stroke.