Study of the mechanism of hemostatic effect of desmopressin

Zubairov, D. M.; Andrushko, I. A.; Zubairova, L. D.; Svintenok, G. Yu.

doi:10.1007/s10517-007-0288-3

Cited by 4 publications

(3 citation statements)

References 9 publications

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“…As shown in Figure 4c, we initially compared CD14 − glyA − LIVE/DEAD ®− CD31 bright CD34 + CD45 − AC133 − events with beads of standardized size in flow cytometry analysis and determined that CD31 bright CD34 + CD45 − AC133 − events were in the range of 1–5µm in size (solid blue in Fig. 4c), which is in the reported size range of extracellular vesicles 31, 37 .…”

Section: Resultsmentioning

confidence: 99%

Flow Cytometric Identification and Functional Characterization of Immature and Mature Circulating Endothelial Cells

Mund

Estes

Yoder

et al. 2012

ATVB

141

125

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Objective We sought to identify and characterize two distinct populations of bona fide circulating endothelial cells, including the endothelial colony forming cell (ECFC), by polychromatic flow cytometry (PFC), colony assays, immunomagnetic selection, and electron microscopy. Methods and Results Mononuclear cells from human umbilical cord blood and peripheral blood were analyzed utilizing our recently published PFC protocol. A population of cells containing both ECFCs and mature circulating endothelial cells (CEC) were determined by varying expressions of CD34, CD31 and CD146, but not AC133 and CD45. After immunomagnetic separation, these cells failed to form hematopoietic colonies, yet clonogenic endothelial colonies with proliferative potential were obtained, thus verifying their identity as ECFCs. The frequency of ECFCs were increased in cord blood and were extremely rare in the peripheral blood of healthy adults. In addition, we also detected another mature endothelial cell population in the circulation that was apoptotic. Finally, when comparing this new protocol to a prior method we determined that the present protocol identifies circulating endothelial cells while the earlier protocol identified extracellular vesicles. Conclusions Two populations of circulating endothelial cells including the functionally characterized ECFC are now identifiable in human cord blood and peripheral blood by PFC.

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Section: Resultsmentioning

confidence: 99%

Flow Cytometric Identification and Functional Characterization of Immature and Mature Circulating Endothelial Cells

Mund

Estes

Yoder

et al. 2012

ATVB

141

125

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“…These V2 receptors have been found to reside in endothelial cells and to lead to the generation of AMPc. Moreover, V2 receptors stimulate the exocytosis of Weibel–Palade bodies, which is where vWF is synthetized, augmenting the factor’s production two- or even threefold [ 197 , 293 , 294 ]. In the case of type II vWD, desmopressin is not indicated, as it may induce thrombosis.…”

Section: Homeostasis-modifying Treatments In Coagulationmentioning

confidence: 99%

The Vascular Endothelium and Coagulation: Homeostasis, Disease, and Treatment, with a Focus on the Von Willebrand Factor and Factors VIII and V

Pablo-Moreno

Serrano

Revuelta

et al. 2022

IJMS

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The vascular endothelium has several important functions, including hemostasis. The homeostasis of hemostasis is based on a fine balance between procoagulant and anticoagulant proteins and between fibrinolytic and antifibrinolytic ones. Coagulopathies are characterized by a mutation-induced alteration of the function of certain coagulation factors or by a disturbed balance between the mechanisms responsible for regulating coagulation. Homeostatic therapies consist in replacement and nonreplacement treatments or in the administration of antifibrinolytic agents. Rebalancing products reestablish hemostasis by inhibiting natural anticoagulant pathways. These agents include monoclonal antibodies, such as concizumab and marstacimab, which target the tissue factor pathway inhibitor; interfering RNA therapies, such as fitusiran, which targets antithrombin III; and protease inhibitors, such as serpinPC, which targets active protein C. In cases of thrombophilia (deficiency of protein C, protein S, or factor V Leiden), treatment may consist in direct oral anticoagulants, replacement therapy (plasma or recombinant ADAMTS13) in cases of a congenital deficiency of ADAMTS13, or immunomodulators (prednisone) if the thrombophilia is autoimmune. Monoclonal-antibody-based anti-vWF immunotherapy (caplacizumab) is used in the context of severe thrombophilia, regardless of the cause of the disorder. In cases of disseminated intravascular coagulation, the treatment of choice consists in administration of antifibrinolytics, all-trans-retinoic acid, and recombinant soluble human thrombomodulin.

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“…Blood for analysis was collected from the femoral artery with Teflon cannulas. Clotting time of fresh arterial blood was evaluated in Bazaron's apparatus [3]. Plasma was separated by 15-min centrifugation of heparin-treated blood at 1500g.…”

mentioning

confidence: 99%

Cell microvesicles during experimental endotoxemia

et al. 2006

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The dynamics of microvesicle formation in arterial blood in generalized Schwartzman phenomenon was studied. Successive (with 24-h interval) intravenous injections of endotoxin to rabbits in a dose of 1 mg/kg and 3 mg/kg caused an increase in the content of microvesicles in the blood, some of them containing ecto-5'-nucleotidase. Biphasic changes in arterial blood clotting time and erythrocyte hemolysis were observed.

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Study of the mechanism of hemostatic effect of desmopressin

Cited by 4 publications

References 9 publications

Flow Cytometric Identification and Functional Characterization of Immature and Mature Circulating Endothelial Cells

Flow Cytometric Identification and Functional Characterization of Immature and Mature Circulating Endothelial Cells

The Vascular Endothelium and Coagulation: Homeostasis, Disease, and Treatment, with a Focus on the Von Willebrand Factor and Factors VIII and V

Cell microvesicles during experimental endotoxemia

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