Agonist-stimulated release of von Willebrand factor and procoagulant factor VIII in rats with and without risk factors for stroke

McCarron, Richard M.; Doron, David A.; Sirén, Anna‐Leena; Feuerstein, Giora; Heldman, Eliahu; Pollard, Harvey B.; Spatz, Maria; Hallenbeck, John M.

doi:10.1016/0006-8993(94)91326-9

Cited by 10 publications

(8 citation statements)

References 33 publications

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“…To address this possibility, we measured vWF secretion as a marker of WPG exocytosis. Again, consistent with the literature [34], LPS increased vWF release from endothelial cells (Fig. 5).…”

Section: Discussionsupporting

confidence: 92%

Ascorbate inhibits platelet-endothelial adhesion in an in-vitro model of sepsis via reduced endothelial surface P-selectin expression

Secor

Swarbreck

Ellis

et al. 2017

Blood Coagulation &Amp; Fibrinolysis

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Plugging of the capillary bed can lead to organ failure and mortality in sepsis. We have reported that intravenous ascorbate injection reduces platelet adhesion to the capillary wall and capillary plugging in septic mice. Both platelet adhesion and capillary plugging require P-selectin, a key adhesion molecule. To elucidate the beneficial effect of ascorbate, we hypothesized that ascorbate reduces platelet-endothelial adhesion by reducing P-selectin surface expression in endothelial cells. We used mouse platelets, and monolayers of cultured microvascular endothelial cells (mouse skeletal muscle origin) stimulated with lipopolysaccharide, to examine platelet-endothelial adhesion. P-selectin mRNA expression in endothelial cells was determined by real-time PCR and P-selectin protein expression at the surface of these cells by immunofluorescence. Secretion of von Willebrand factor from cells into the supernatant (a measure of P-selectin-containing granule exocytosis) was determined by ELISA. Lipopolysaccharide (10 μg/ml, 1 h) increased platelet-endothelial adhesion. P-selectin-blocking antibody inhibited this adhesion. Lipopolysaccharide also increased P-selectin mRNA in endothelial cells, P-selectin expression at the endothelial surface, and von Willebrand factor secretion. Ascorbate pretreatment (100 μmol/l, 4 h) inhibited the increased platelet adhesion, surface expression of P-selectin, and von Willebrand factor secretion, but not the increase in P-selectin mRNA. The lipopolysaccharide-induced increase in platelet-endothelial adhesion requires P-selectin presence at the endothelial surface. Ascorbate's ability to reduce this presence could be important in reducing both platelet adhesion to the capillary wall and capillary plugging in sepsis.

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Section: Discussionsupporting

confidence: 92%

Ascorbate inhibits platelet-endothelial adhesion in an in-vitro model of sepsis via reduced endothelial surface P-selectin expression

Secor

Swarbreck

Ellis

et al. 2017

Blood Coagulation &Amp; Fibrinolysis

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“…An increased concentration of adhesive protein vWF 23 and increased fibrinogen binding 7 in SHRs is another plausible mechanism for hypertension-induced enhanced thrombogenesis in the response to acute focal injury. Although vWF is thought to have a greater effect at higher wall shear rates (arterioles), 24,25 our previous results, 26 in agreement with Ross et al, 25 have shown vWF's importance at lower wall shear rates as well.…”

Section: Discussionmentioning

confidence: 99%

In Vivo Platelet Thrombus Formation in Microvessels of Spontaneously Hypertensive Rats

Lominadze

Joshua

Schuschke

1997

American Journal of Hypertension

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Sustained high blood pressure causes functional changes in both vascular endothelial cells and platelets. Therefore, we hypothesized that in vivo platelet thrombus formation would be increased in the cremaster muscle microvessels of rats during genetic hypertension. Experiments were carried out on spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) at 12 weeks of age. Fluorescein isothiocyanate tagged to bovine serum albumin (FITC-BSA) was injected intraarterially and 450 to 490 nm light was used to activate the FITC-BSA and induce a thrombus within the vasculature. In vivo television microscopy was used to quantitate thrombus formation and microvascular diameter changes. The time of platelet thrombus initiation and subsequent time of thrombus growth were studied at wall shear rates of approximately 2000 sec ؊1 and 270 sec ؊1 in third-order arterioles and venules, respectively. In SHR, times for platelet thrombus initiation and vessel occlusion were significantly less in both arterioles and venules, whereas time for platelet thrombus growth following initiation was significantly prolonged. Greater shear rates in arterioles compared to venules decreased platelet adhesion and subsequently decreased the rate of thrombus formation in both WKY and SHR groups. However, the ratio of WKY to SHR platelet thrombus growth (platelet aggregation) time remained similar (0.83 ؎ 0.06 in arterioles and 0.79 ؎ 0.06 in venules). These results indicate that there is increased thrombus formation during hypertension and that the platelet adhesion processes may be of greater importance than platelet aggregation in producing this increase. Am

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“…In rats, increased vWF expression has been demonstrated immunohistochemically in regenerating vascular endothelium after endotoxin damage, after balloon catheterization (23), or during the development of irradiation-induced pulmonary fibrosis (11). Increases in plasma vWF within minutes of insult have been reported in rats after being rendered hypotonic by intravenously administered water (5), with microscopic evidence of endothelial damage as well as in rats given endotoxin (17) or in isolated perfused rat lungs (9). Interestingly, studies have rarely employed morphological assessment of endothelial cell integrity.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Plasma von Willebrand Factor as a Biomarker for Acute Arterial Damage in Rats

et al. 2000

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Agonist-stimulated release of von Willebrand factor and procoagulant factor VIII in rats with and without risk factors for stroke

Cited by 10 publications

References 33 publications

Ascorbate inhibits platelet-endothelial adhesion in an in-vitro model of sepsis via reduced endothelial surface P-selectin expression

Ascorbate inhibits platelet-endothelial adhesion in an in-vitro model of sepsis via reduced endothelial surface P-selectin expression

In Vivo Platelet Thrombus Formation in Microvessels of Spontaneously Hypertensive Rats

Evaluation of Plasma von Willebrand Factor as a Biomarker for Acute Arterial Damage in Rats

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