Thrombospondin 1 requires von Willebrand factor to modulate arterial thrombosis in mice

Prakash, Prem; Kulkarni, Paresh P.; Chauhan, Anil K.

doi:10.1182/blood-2014-06-581942

Cited by 36 publications

(33 citation statements)

References 49 publications

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“…27 In brief, recipient mice were irradiated with 2 doses of 6.5 Gy at an interval of 4 hours between the first and second irradiations. Bone marrow cells were sterilely extracted from excised femurs and tibias of euthanized Fn-EDA Figure 3; FACSCalibur, BD Biosciences).…”

Section: Bmtmentioning

confidence: 99%

“…We used a recent elegant adoptive platelet transfer method, 27,36 which allowed us to rapidly generate Fn-EDA 1/1 mice lacking TLR4 only in platelets. We performed transplantation of bone marrow from GPIba/human IL4R transgenic mice into Fn-EDA 1/1 mice and characterized the hematopoietic phenotype by flow cytometry (supplemental Figure 4).…”

Section: Cellular Fn-eda1 Potentiates Platelet Aggregation Through Tlr4mentioning

confidence: 99%

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Cellular fibronectin containing extra domain A promotes arterial thrombosis in mice through platelet Toll-like receptor 4

Prakash

Kulkarni

Lentz

et al. 2015

Blood

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Section: Bmtmentioning

confidence: 99%

Section: Cellular Fn-eda1 Potentiates Platelet Aggregation Through Tlr4mentioning

confidence: 99%

Cellular fibronectin containing extra domain A promotes arterial thrombosis in mice through platelet Toll-like receptor 4

Prakash

Kulkarni

Lentz

et al. 2015

Blood

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“…For dual-visualization of platelets and fibrin, rhodamine B-labeled platelets were injected with Alexa-488 labeled anti-fibrin antibody (2 mg/kg) via the retro-orbital plexus 39 in anesthetized mice. To measure PS exposure, mice were subjected to IVC flow restriction for 3 hours received through a jugular vein catheter Alexa Fluor 647 conjugated Annexin V (20 mg per mouse) and fluorescein isothiocyanate anti-mouse Gr-1 1 (6 mL per mouse).…”

Section: Tail-bleeding Assay and Inferior Vena Cava (Ivc) Flow Restrimentioning

confidence: 99%

Distinct contributions of complement factors to platelet activation and fibrin formation in venous thrombus development

Subramaniam

Jurk

Hobohm

et al. 2017

Blood

205

188

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• Myeloid cell TF-dependent venous thrombosis is under control of PDI and the complement cascade.• C5 deficiency reduces fibrin formation and leukocyte PS exposure with normal platelet deposition in flow-restricted vessels.Expanding evidence indicates multiple interactions between the hemostatic system and innate immunity, and the coagulation and complement cascades. Here we show in a tissue factor (TF)-dependent model of flow restriction-induced venous thrombosis that complement factors make distinct contributions to platelet activation and fibrin deposition. Complement factor 3 (C3) deficiency causes prolonged bleeding, reduced thrombus incidence, thrombus size, fibrin and platelet deposition in the ligated inferior vena cava, and diminished platelet activation in vitro. Initial fibrin deposition at the vessel wall over 6 hours in this model was dependent on protein disulfide isomerase (PDI) and TF expression by myeloid cells, but did not require neutrophil extracellular trap formation involving peptidyl arginine deiminase 4. In contrast to C3 2/2 mice, C5-deficient mice had no apparent defect in platelet activation in vitro, and vessel wall platelet deposition and initial hemostasis in vivo. However, fibrin formation, the exposure of negatively charged phosphatidylserine (PS) on adherent leukocytes, and clot burden after 48 hours were significantly reduced in C5 2/2 mice compared with wild-type controls. These results delineate that C3 plays specific roles in platelet activation independent of formation of the terminal complement complex and provide in vivo evidence for contributions of complement-dependent membrane perturbations to prothrombotic TF activation on myeloid cells. (Blood. 2017;129(16):2291-2302

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“…Approximately 30% of mice showed a recovery of WBC number to the normal range of 2.6-10×10 3 /µL after treatment with IRAK/ABT-NP. 32 The WBC data suggest that IRAK/ABT-NP could better improve lymphoid blast in T-ALL mouse model than other formulations. To confirm the improved efficacy of IRAK/ABT-NP in the treatment of T-ALL mouse model, smears of peripheral blood from each group were prepared to check preliminary impression of numbers of lymphoblastic leukemia cells after 4 weeks' treatment.…”

Section: Efficacy In Pdx Mouse Modelmentioning

confidence: 99%

Cooperation of IRAK1/4 inhibitor and ABT-737 in nanoparticles for synergistic therapy of T cell acute lymphoblastic leukemia

Wu¹,

Wang²,

Qiu³

et al. 2017

IJN

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T cell acute lymphoblastic leukemia (T-ALL) is caused by clonal expansion of variant T cell progenitors and is considered as a high risk leukemia. Contemporary single chemotherapy has a limited effect due to dynamic and versatile properties of T-ALL. Here IRAK1/4 inhibitor and ABT-737 were co-encapsulated into polyethylene glycol modified poly (lactic-co-glycolic acid) nanoparticles (IRAK/ABT-NP) to enhance synergistic therapy of T-ALL. The formulation was optimized to achieve high drug loading using Box-Behnken design and response surface methodology. The optimal parameter comprised 2.98% polymer in acetonitrile, a ratio of oil phase to water phase of 1:8.33, and 2.12% emulsifier concentration. High drug loading and uniform spherical shape was achieved. In vitro release study showed sustained release of IRAK1/4 inhibitor for 72 hours as well as sustained release of ABT-737 for more than 120 hours. Uptake efficiency of IRAK/ABT-NP and induced apoptotic T-ALL fraction by IRAK/ABT-NP were much higher than the IRAK1/4 and ABT-737 combined solution. IC 50 of IRAK/ABT-NP was two-fold lower than free drug combination in Jurkat cells. Additionally, we conducted in vivo experiments in which IRAK/ABT-NP exhibited greater cytotoxicity toward T-ALL cells, the capacity to significantly restore white blood cell number in peripheral blood, and improved survival time of T-ALL mouse model compared to the IRAK1/4 and ABT-737 combined solution.

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Thrombospondin 1 requires von Willebrand factor to modulate arterial thrombosis in mice

Abstract: Key Points Thrombospondin 1 requires the presence of VWF to modulate arterial thrombosis. Platelet thrombospondin 1 contributes to arterial thrombosis.

Cited by 36 publications

References 49 publications

Cellular fibronectin containing extra domain A promotes arterial thrombosis in mice through platelet Toll-like receptor 4

Cellular fibronectin containing extra domain A promotes arterial thrombosis in mice through platelet Toll-like receptor 4

Distinct contributions of complement factors to platelet activation and fibrin formation in venous thrombus development

Cooperation of IRAK1/4 inhibitor and ABT-737 in nanoparticles for synergistic therapy of T cell acute lymphoblastic leukemia

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