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CLIC1 Cooperates with Integrins to Promote Thrombus Formation and Angiogenesis
Chloride intracellular channel 1 (CLIC1) is a member of a family of six highly homologous membrane proteins (CLIC1-6), which have been shown to be co-regulated with integrins suggesting their involvement in cell adhesion, migration and proliferation. CLIC1 is a metamorphic protein that functions as an oxidoreductase in the cytoplasm as well as an ion channel in the cell membrane. CLIC1 is upregulated in angiogenic endothelial and metastatic tumor cells. In addition, studies in CLIC1 knockout mice have shown that CLIC1 promotes platelet function. Here, we hypothesize that CLIC1 supports cell adhesive functions in platelets ...
Source: Blood - November 21, 2018 Category: Hematology Authors: Knowles, L. M., Ampofo, E., Menger, M. D., Niewald, P., Drawz, A., Eichler, H., Pilch, J. Tags: 301. Vascular Wall Biology, Endothelial Progenitor Cells, and Platelet Adhesion, Activation, and Biochemistry: Poster II Source Type: research

A Critical Role of Growth Arrest-Specific Gene 6-Mer Axis in the Pathogenesis of Endothelial Damage Contributing to Thrombotic Microangiopathy Associated with Graft-Versus-Host Disease after Allogeneic Hematopoietic Stem Cell Transplantation
Graft-versus-host disease (GVHD) and thrombotic microangiopathy (TMA) are severe complications of allogeneic hematopoietic stem cell transplantation (allo-SCT). Host endothelial cells are targets of alloreactive donor cytotoxic T lymphocytes or various proinflammatory cytokines following allo-SCT, and endothelial damage plays an important role in the pathogenic mechanism(s) of TMA associated with GVHD. However, the detailed mechanism(s) of TMA as well as GVHD have not yet been fully elucidated. Growth arrest-specific (Gas) 6 structurally belongs to the family of plasma vitamin K-dependent proteins working as a cofactor for...
Source: Blood - November 21, 2018 Category: Hematology Authors: Furukawa, M., Xintao, W., Ohkawara, H., Fukatsu, M., Alkebsi, L., Noji, H., Ogawa, K., Ikezoe, T. Tags: 701. Experimental Transplantation: Basic Biology, Pre-Clinical Models: Poster III Source Type: research

Role of platelets, neutrophils, and factor XII in spontaneous venous thrombosis in mice
This study challenges the proposed roles of neutrophils and FXII in venous thrombosis pathophysiology.
Source: Blood - May 25, 2016 Category: Hematology Authors: Heestermans, M., Salloum-Asfar, S., Salvatori, D., Laghmani, E. H., Luken, B. M., Zeerleder, S. S., Spronk, H. M. H., Korporaal, S. J., Wagenaar, G. T. M., Reitsma, P. H., van Vlijmen, B. J. M. Tags: Phagocytes, Granulocytes, and Myelopoiesis, Platelets and Thrombopoiesis, Thrombosis and Hemostasis Source Type: research

G protein-dependent basal and evoked endothelial cell vWF secretion
von Willebrand factor (vWF) secretion by endothelial cells (ECs) is essential for hemostasis and thrombosis; however, the molecular mechanisms are poorly understood. Interestingly, we observed increased bleeding in EC-Gα13–/–;Gα12–/– mice that could be normalized by infusion of human vWF. Blood from Gα12–/– mice exhibited significantly reduced vWF levels but normal vWF multimers and impaired laser-induced thrombus formation, indicating that Gα12 plays a prominent role in EC vWF secretion required for hemostasis and thrombosis. In isolated buffer-perfused mouse lun...
Source: Blood - January 16, 2014 Category: Hematology Authors: Rusu, L., Andreeva, A., Visintine, D. J., Kim, K., Vogel, S. M., Stojanovic-Terpo, A., Chernaya, O., Liu, G., Bakhshi, F. R., Haberichter, S. L., Iwanari, H., Kusano-Arai, O., Suzuki, N., Hamakubo, T., Kozasa, T., Cho, J., Du, X., Minshall, R. D. Tags: Thrombosis and Hemostasis, Vascular Biology Source Type: research

Prolylcarboxypeptidase promotes angiogenesis and vascular repair
Prolylcarboxypeptidase (PRCP) is associated with leanness, hypertension, and thrombosis. PRCP-depleted mice have injured vessels with reduced Kruppel-like factor (KLF)2, KLF4, endothelial nitric oxide synthase (eNOS), and thrombomodulin. Does PRCP influence vessel growth, angiogenesis, and injury repair? PRCP depletion reduced endothelial cell growth, whereas transfection of hPRCP cDNA enhanced cell proliferation. Transfection of hPRCP cDNA, or an active site mutant (hPRCPmut) rescued reduced cell growth after PRCP siRNA knockdown. PRCP-depleted cells migrated less on scratch assay and murine PRCPgt/gt aortic segments had ...
Source: Blood - August 22, 2013 Category: Hematology Authors: Adams, G. N., Stavrou, E. X., Fang, C., Merkulova, A., Alaiti, M. A., Nakajima, K., Morooka, T., Merkulov, S., LaRusch, G. A., Simon, D. I., Jain, M. K., Schmaier, A. H. Tags: Vascular Biology Source Type: research

Acute and severe coagulopathy in adult mice following silencing of hepatic antithrombin and protein C production
Mice deficient in the anticoagulants antithrombin (Serpinc1) or protein C (Proc) display premature death due to thrombosis-related coagulopathy, thereby precluding their use in gene function studies and thrombosis models. We used RNA interference to silence Serpinc1 and/or Proc in normal adult mice. The severe coagulopathy that followed combined "knockdown" of these genes is reported. Two days after siRNA injection, thrombi (occlusive) were observed in vessels (large and medium-sized) in multiple tissues, and hemorrhages were prominent in the ocular, mandibular, and maxillary areas. Tissue fibrin deposition and reduction o...
Source: Blood - May 23, 2013 Category: Hematology Authors: Safdar, H., Cheung, K. L., Salvatori, D., Versteeg, H. H., Laghmani, E. H., Wagenaar, G. T. M., Reitsma, P. H., van Vlijmen, B. J. M. Tags: Thrombosis and Hemostasis, Brief Reports Source Type: research