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Thrombin receptor PAR1 silencing in endothelial colony forming cells modifies stemness and vasculogenic properties
CONCLUSIONS: In conclusion, our work describes for the first time a link between PAR1, stemness and vasculogenesis in human ECFCs.PMID:37678550 | DOI:10.1016/j.jtha.2023.08.029
Source: Thrombosis and Haemostasis - September 7, 2023 Category: Hematology Authors: David M Smadja Elisa Rossi Skerdi Haviari Ivan Bieche Audrey Cras Pascale Gaussem Source Type: research

Assessment of breast cancer progression and metastasis during a hypercoagulable state induced by silencing of antithrombin in a xenograft mouse model
Local coagulation activation has been shown to impact both primary tumor growth and metastasis in mice. It is well known that components of the blood clotting cascade such as tissue factor and thrombin play a role in tumor progression by activating cellular receptors and local formation of fibrin. However, whether venous thromboembolism (VTE) or a hypercoagulable state has a direct impact on cancer progression is unknown. Here we have combined an orthotopic murine breast cancer model, using female Nod-SCID mice, with siRNA-mediated silencing of antithrombin (siAT) leading to the induction of a systemic hypercoagulable state.
Source: Thrombosis Research - November 24, 2022 Category: Hematology Authors: J.T. Buijs, B. Ünlü, E.H. Laghmani, M. Heestermans, B.J.M. van Vlijmen, H.H. Versteeg Tags: Full Length Article Source Type: research

Elimination of fibrin polymer formation or crosslinking, but not fibrinogen deficiency, is protective against diet-induced obesity and associated pathologies
CONCLUSIONS: Consistent with prior studies, Fib𝛾390-396A mice were significantly protected from increased adiposity, NAFLD, hypercholesterolemia and diabetes while Fib- and siFga-treated mice gained as much weight and developed obesity-associated pathologies identical to wildtype mice. FibAEK and FXIII- mice displayed an intermediate phenotype with partial protection from some obesity-associated pathologies. Results here indicate that fibrin(ogen) lacking αM β2 binding function offers substantial protection from obesity and associated disease that is partially recapitulated by preventing fibrin polymer formation or cr...
Source: Thrombosis and Haemostasis - September 16, 2022 Category: Hematology Authors: Woosuk S Hur Katharine C King Yesha N Patel Y-Van Nguyen Zimu Wei Yi Yang Lih Jiin Juang Jerry Leung Christian J Kastrup Alisa S Wolberg James P Luyendyk Matthew J Flick Source Type: research

Protein Tyrosine Phosphatase 1B Deficiency in Vascular Smooth Muscle Cells Promotes Perivascular Fibrosis following Arterial Injury
CONCLUSION: Chronic reduction of PTP1B in SMCs promotes dedifferentiation, perivascular fibrosis, and adverse remodeling following vascular injury by mechanisms involving an ERK1/2 phosphorylation-driven shift from SMAD2 to KLF4-regulated gene transcription.PMID:36075234 | DOI:10.1055/s-0042-1755329
Source: Thrombosis and Haemostasis - September 8, 2022 Category: Hematology Authors: Rajinikanth Gogiraju Sogol Gachkar David Velmeden Magdalena L Bochenek Konstantinos Zifkos Astrid Hubert Thomas M ünzel Stefan Offermanns Katrin Sch äfer Source Type: research

Osteoprotegerin modulates platelet adhesion to von Willebrand factor during release from endothelial cells
CONCLUSIONS: Release of VWF from endothelial cells opens the platelet-binding site, irrespective of the presence of flow. However, not all available platelet-binding sites are being occupied, suggesting some extent of regulation. Part of this regulation involves endothelial proteins that are co-secreted with VWF, like osteoprotegerin. This regulatory mechanism may be of more relevance under inflammatory conditions.PMID:34816579 | DOI:10.1111/jth.15598
Source: Thrombosis and Haemostasis - November 24, 2021 Category: Hematology Authors: Nikolett Wohner Silvie Sebastian Vincent Muczynski Dana Huskens Bas de Laat Philip G de Groot Peter J Lenting Source Type: research

Targeting of antithrombin in hemophilia A or B with investigational siRNA therapeutic fitusiran - results of the phase 1 inhibitor cohort.
CONCLUSIONS: Monthly fitusiran was generally well tolerated, lowered antithrombin levels from baseline, and resulted in improved thrombin generation. These preliminary results suggest that monthly fitusiran treatment may reduce bleeding episodes and improve QoL in participants with hemophilia A or B with inhibitors. PMID: 33587824 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - February 15, 2021 Category: Hematology Authors: Pasi KJ, Lissitchkov T, Mamonov V, Mant T, Timofeeva M, Bagot C, Chowdary P, Georgiev P, Gercheva-Kyuchukova L, Madigan K, Nguyen H, Yu Q, Mei B, Benson CC, Ragni MV Tags: J Thromb Haemost Source Type: research

Knockdown of liver-derived factor XII by GalNAc-siRNA ALN-F12 prevents thrombosis in mice without impacting hemostatic function
Plasma coagulation Factor XII (FXII) plays a crucial role in contact activation, ultimately regulating both the kinin-kallikrein system and the intrinsic pathway of coagulation. A growing body of evidence suggests that inhibition of FXII can prevent thrombosis. Given FXII does not appear to modulate hemostasis, targeting FXII is a promising strategy for the prevention of pathological thrombus formation without the hemostatic risks typically associated with anticoagulants. To this end, a subcutaneously administered investigational RNAi therapeutic targeting liver F12 mRNA (ALN-F12) was developed.
Source: Thrombosis Research - August 26, 2020 Category: Hematology Authors: Jingxuan Liu, Brian C. Cooley, Akin Akinc, James Butler, Anna Borodovsky Tags: Full Length Article Source Type: research

Ex vivo Improvement of a von Willebrand Disease Type 2A Phenotype Using an Allele-Specific Small-Interfering RNA.
Abstract Von Willebrand disease (VWD) is the most common inherited bleeding disorder and is mainly caused by dominant-negative mutations in the multimeric protein von Willebrand factor (VWF). These mutations may either result in quantitative or qualitative defects in VWF. VWF is an endothelial protein that is secreted to the circulation upon endothelial activation. Once secreted, VWF multimers bind platelets and chaperone coagulation factor VIII in the circulation. Treatment of VWD focuses on increasing VWF plasma levels, but production and secretion of mutant VWF remain uninterrupted. Presence of circulating muta...
Source: Thrombosis and Haemostasis - August 14, 2020 Category: Hematology Authors: de Jong A, Dirven RJ, Boender J, Atiq F, Anvar SY, Leebeek FWG, van Vlijmen BJM, Eikenboom J Tags: Thromb Haemost Source Type: research

Hypoxia induced up-regulation of tissue factor is mediated through extracellular RNA activated Toll-like receptor 3-activated protein 1 signalling.
Abstract Sterile Inflammation (SI), a condition where damage associated molecular patterns (DAMPs) released from dying cells, leads to TLR (Toll-like receptor) activation and triggers hypoxemia in circulation leading to venous thrombosis (VT) through tissue factor (TF) activation, but its importance under acute hypoxia (AH) remains unexplored. Thus, we hypothesized that eRNA released from dying cells under AH activates TF via the TLR3-ERK1/2-AP1 pathway, leading to VT. Animals were exposed to stimulate hypoxia for 0-24 h at standard temperature and humidity. RNaseA and DNase1 were injected immediately before expo...
Source: Blood Cells, Molecules and Diseases - June 10, 2020 Category: Hematology Authors: Bhagat S, Biswas I, Ahmed R, Khan GA Tags: Blood Cells Mol Dis Source Type: research

SLC44A2 deficient mice have a reduced response in stenosis but not in hypercoagulability driven venous thrombosis.
CONCLUSIONS: These studies corroborate the original GWAS findings and establish a contributing role for SLC44A2 during the initiation of VT, with indications that this may be related to platelet-neutrophil interaction. The precise mechanism however remains elusive and warrants further investigation. PMID: 32297475 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - April 14, 2020 Category: Hematology Authors: Tilburg J, Coenen DM, Zirka G, Dólleman S, van Oeveren-Rietdijk AM, Karel MFA, de Boer HC, Cosemans JMEM, Versteeg HH, Morange PE, van Vlijmen BJM, Maracle CX, Thomas GM Tags: J Thromb Haemost Source Type: research

Plasmodium falciparum histidine rich protein HRPII inhibits the antiinflammatory function of antithrombin.
CONCLUSION: We postulate that Pf-derived HRPII and polyphosphate can contribute to the pathogenesis of malaria infection by downregulating the AT-dependent antiinflammatory and anticoagulant pathways. PMID: 31858717 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - December 18, 2019 Category: Hematology Authors: Dinarvand P, Yang L, Biswas I, Giri H, Rezaie AR Tags: J Thromb Haemost Source Type: research

P14. Abstract Title: Modulating Fibrinolysis using siRNA against Coagulation Factor XIII
High specificity, easy reversibility, and a half-life on the order of weeks; these are all major advantages that gene therapy has over traditional anticoagulants, add to that a strategy that weakens clots rather than preventing clotting altogether and prophylaxis of thrombosis may become much safer. Currently, anticoagulant drugs are used as a preventative measure for people susceptible to developing disease causing thrombi (which manifest as heart attacks, strokes, and pulmonary embolism), but they require frequent administration and their strict inhibition of clotting increases the risk of uncontrolled bleeding.
Source: Thrombosis Research - September 30, 2019 Category: Hematology Authors: A. Strilchuk, E. Conway, E. Pryzdial, P. Cullis, C. Kastrup Source Type: research

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