Filtered By:
Specialty: Hematology

This page shows you your search results in order of date. This is page number 10.

Order by Relevance | Date

Total 236 results found since Jan 2013.

Gas6 regulates thrombin‐induced expression of VCAM‐1 through FoxO‐1 in endothelial cells
This article is protected by copyright. All rights reserved.
Source: Journal of Thrombosis and Haemostasis - September 28, 2015 Category: Hematology Authors: F.R. Bertin, C.A. Lemarié, R.S. Robins, M.D. Blostein Tags: Original Article ‐ Vascular Biology Source Type: research

Gas6 regulates thrombin-induced expression of VCAM-1 through FoxO-1 in endothelial cells.
CONCLUSIONS: Thrombin induces VCAM-1 expression as well as FoxO-1 phosphorylation and nuclear exclusion in WT ECs only. Silencing FoxO-1 enhances VCAM-1 expression in both WT and Gas6(-/-) ECs. Inhibition of Akt or FoxO-1 phosphorylation prevents VCAM-1 expression in WT ECs. These data show that Gas6 induces FoxO-1 phosphorylation leading to de-repression of VCAM-1 expression. BM-MC/EC adhesion is increased by thrombin in WT ECs. BM-MC/EC adhesion is further increased when FoxO-1 is silenced but decreased when FoxO-1 phosphorylation is inhibited. These results demonstrate that the Gas6/FoxO-1 signaling axis plays an import...
Source: Thrombosis and Haemostasis - September 28, 2015 Category: Hematology Authors: Bertin FR, Lemarié CA, Robins RS, Blostein MD Tags: J Thromb Haemost Source Type: research

Rapamycin restores p14, p15 and p57 expression and inhibits the mTOR/p70S6K pathway in acute lymphoblastic leukemia cells.
Abstract The aim of the present study was to investigate the effects of rapamycin and its underlying mechanisms on acute lymphoblastic leukemia (ALL) cells. We found that the p14, p15, and p57 genes were not expressed in ALL cell lines (Molt-4 and Nalm-6) and adult ALL patients, whereas mTOR, 4E-BP1, and p70S6K were highly expressed. In Molt-4 and Nalm-6 cells exposed to rapamycin, cell viability decreased and the cell cycle was arrested at the G1/S phase. Rapamycin restored p14, p15, and p57 gene expression through demethylation of the promoters of these genes. As expected, rapamycin also increased p14 and p15 pr...
Source: International Journal of Hematology - September 11, 2015 Category: Hematology Authors: Li H, Kong X, Cui G, Ren C, Fan S, Sun L, Zhang Y, Cao R, Li Y, Zhou J Tags: Int J Hematol Source Type: research

A Novel Pathway of Cellular Activation Mediated by Antiphospholipid Antibody-Induced Extracellular Vesicles.
CONCLUSIONS: Anti-β2GPI antibodies caused formation of an endothelial cell inflammasome and release of EV that were enriched in mature IL-1β, had a distinct miRNA profile, and caused endothelial activation. However, activation was not inhibited by an IL-1β antibody, IL-1 receptor antagonist or IL-1 receptor siRNA. Endothelial cell activation by EV required IRAK4 phosphorylation and was inhibited by pretreatment of cells with TLR7 siRNA or RNase A, which degrades single-stranded RNA. Profiling of miRNA in EV released from endothelial cells incubated with β2GPI and either control IgG or anti-β2GPI antibodies revealed nu...
Source: Thrombosis and Haemostasis - August 12, 2015 Category: Hematology Authors: Wu M, Barnard J, Kundu S, McCrae KR Tags: J Thromb Haemost Source Type: research

A Novel Pathway of Cellular Activation Mediated by Antiphospholipid Antibody‐Induced Extracellular Vesicles
ConclusionsAnti‐β2GPI antibodies caused formation of an endothelial cell inflammasome and release of EV that were enriched in mature IL‐1β, had a distinct miRNA profile, and caused endothelial activation. However, activation was not inhibited by an IL‐1β antibody, IL‐1 receptor antagonist or IL‐1 receptor siRNA. Endothelial cell activation by EV required IRAK4 phosphorylation and was inhibited by pretreatment of cells with TLR7 siRNA or RNase A, which degrades single‐stranded RNA. Profiling of miRNA in EV released from endothelial cells incubated with β2GPI and either control IgG or anti‐β2GPI antibodies...
Source: Journal of Thrombosis and Haemostasis - August 12, 2015 Category: Hematology Authors: M. Wu, J. Barnard, S. Kundu, KR McCrae Tags: Original Article ‐ Vascular Biology Source Type: research

Antineoplastic effects of liposomal siRNA treatment targeting BLIMP1/PRDM1 in primary effusion lymphoma.
PMID: 26206802 [PubMed - as supplied by publisher]
Source: Haematologica - July 23, 2015 Category: Hematology Authors: Riva G, Lagreca I, Mattiolo A, Belletti D, Lignitto L, Barozzi P, Ruozi B, Vallerini D, Quadrelli C, Corradini G, Forghieri F, Marasca R, Narni F, Tosi G, Forni F, Vandelli MA, Amadori A, Chieco-Bianchi L, Potenza L, Calabro' ML, Luppi M Tags: Haematologica Source Type: research

Silencing of protease‐activated receptors attenuates synovitis and cartilage damage following a joint bleed in haemophilic mice
ConclusionThis study demonstrates that synovial and chondrocyte PAR expression is altered upon a joint bleed, and that treatment with PAR1–4 siRNA attenuates synovitis and plasmin‐induced cartilage damage.
Source: Haemophilia - July 1, 2015 Category: Hematology Authors: L. Nieuwenhuizen, R. E. G. Schutgens, K. Coeleveld, S. C. Mastbergen, R. M. Schiffelers, G. Roosendaal, D. H. Biesma, F. P. J. G. Lafeber Tags: Original Article Source Type: research

Treprostinil indirectly regulates endothelial colony forming cell angiogenic properties by increasing VEGF-A produced by mesenchymal stem cells.
In conclusion, increased VEGF-A produced by MSC can account for the increased vessel formation observed during treprostinil treatment. The clinical relevance of these data was confirmed by the high level of VEGF-A detected in plasma from patients with paediatric PH who had been treated with treprostinil. Moreover, our results suggest that VEGF-A level in patients could be a surrogate biomarker of treprostinil efficacy. PMID: 26062754 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - June 11, 2015 Category: Hematology Authors: Smadja DM, Levy M, Huang L, Rossi E, Blandinieres A, Israël-Biet D, Gaussem P, Bischoff J Tags: Thromb Haemost Source Type: research

Accumulation of tissue factor in endothelial cells induces cell apoptosis, mediated through p38 and p53 activation.
In conclusion, accumulation of TF within endothelial cell, or sequestered from the surrounding can induce cellular apoptosis through mechanisms mediated by p38, and involves the stabilisation of p53. PMID: 25903973 [PubMed - as supplied by publisher]
Source: Thrombosis and Haemostasis - April 23, 2015 Category: Hematology Authors: ElKeeb AM, Collier ME, Maraveyas A, Ettelaie C Tags: Thromb Haemost Source Type: research

DUSP4-mediated accelerated T-cell senescence in idiopathic CD4 lymphopenia
Idiopathic CD4 lymphopenia (ICL) is a rare heterogeneous immunological syndrome of unclear etiology. ICL predisposes patients to severe opportunistic infections and frequently leads to poor vaccination effectiveness. Chronic immune activation, expansion of memory T cells, and impaired T-cell receptor (TCR) signaling have been reported in ICL, but the mechanistic and causative links remain unclear. We show that late-differentiated T cells in 20 patients with ICL displayed defective TCR responses and aging markers similar to those found in T cells from elderly subjects. Intrinsic T-cell defects were caused by increased expre...
Source: Blood - April 16, 2015 Category: Hematology Authors: Bignon, A., Regent, A., Klipfel, L., Desnoyer, A., de la Grange, P., Martinez, V., Lortholary, O., Dalloul, A., Mouthon, L., Balabanian, K. Tags: Immunobiology Source Type: research

NMMHCIIA inhibition impedes tissue factor expression and venous thrombosis via Akt/GSK3β-NF-κB signalling pathways in the endothelium.
Abstract Non-muscle myosin heavy chain IIA (NMMHC IIA) has been shown to be involved in thrombus formation and inflammatory microparticle release in endothelial cells. However, the role of NMMHC IIA in regulating the expression of tissue factor (TF) and deep venous thrombosis remains to be elucidated. In the present study, endothelial cells were stimulated with tumour necrosis factor-α (TNF-α) to induce TF expression. Pretreatment with the NMMHC II inhibitor blebbistatin suppressed the mRNA and protein expressions as well as the procoagulant activity of TF in a dose-dependent manner. Blebbistatin enhanced Akt an...
Source: Thrombosis and Haemostasis - April 16, 2015 Category: Hematology Authors: Zhai K, Tang Y, Zhang Y, Li F, Wang Y, Cao Z, Yu J, Kou J, Yu B Tags: Thromb Haemost Source Type: research

Mammalian target of rapamycin complex 2 (mTORC2) regulates LPS-induced expression of IL-12 and IL-23 in human dendritic cells.
Abstract IL-12 p40, a common subunit for both IL-12 p70 and IL-23, plays a critical role in the development of Th1 and Th17 cells and autoimmune diseases. Regulation of IL-12 p40 expression is thus considered to be a strategy for developing therapies for Th1- and Th17-mediated autoimmune diseases. The mTOR protein is a subunit mTORC1 and mTORC2. Although mTORC1 has been shown to mediate IL-12 p40 expression in DCs and relevant signaling, the role of mTORC2 in IL-12 p40 expression remains largely unclear. In the present study, we demonstrate that blocking mTORC2 activity using the phytochemical cytopiloyne can spec...
Source: Journal of Leukocyte Biology - April 15, 2015 Category: Hematology Authors: Wei WC, Liu CP, Yang WC, Shyur LF, Sheu JH, Chen SS, Yang NS Tags: J Leukoc Biol Source Type: research

Inorganic polyphosphate elicits pro‐inflammatory responses through activation of the mammalian target of rapamycin complexes 1 and 2 in vascular endothelial cells
ConclusionsPolyP, through interaction with RAGE and P2Y1, activates both the mTORC1 and mTORC2 signaling network. Both the pro‐inflammatory and mTOR signaling functions of polyP are linked.
Source: Journal of Thrombosis and Haemostasis - April 13, 2015 Category: Hematology Authors: S. M. Hassanian, P. Dinarvand, S. A. Smith, A. R. Rezaie Tags: Original Article Source Type: research

Alteration of gene expression profile following PPP2R5C knockdown may be associated with proliferation suppression and increased apoptosis of K562 cells
In this study, we further characterized the gene expression profiles after PPP2R5C suppression by microarray analysis. Genes which participate in the MAPK, PI3K/AKT, and JAK/STAT pathways, were mainly altered in the K562 cells. We propose that the mechanism for proliferation inhibition and increased apoptosis of K562 cells following PPP2R5C suppression may be related to the alteration of expression profiles of BRAF, AKT2, AKT3, NFKB2 and STAT3 genes.
Source: Journal of Hematology and Oncology - April 12, 2015 Category: Hematology Authors: Sichu LiuQi ShenYu ChenChengwu ZengChangshu CaoLijiang YangShaohua ChenXiuli WuBo LiYangqiu Li Source Type: research

Titrating haemophilia B phenotypes using siRNA strategy: evidence that antithrombotic activity is separated from bleeding liability.
Abstract Haemophilia A and B are characterised by a life-long bleeding predisposition, and several lines of evidence suggest that risks of atherothrombotic events may also be reduced. Establishing a direct correlation between coagulation factor levels, thrombotic risks and bleeding propensity has long been hampered by an inability to selectively and specifically inhibit coagulation factor levels. Here, the exquisite selectivity of gene silencing combined with a gene knockout (KO) approach was used to define the relative contribution of factor IX (fIX) to thrombosis and primary haemostasis in the rat. Using a lipid...
Source: Thrombosis and Haemostasis - March 19, 2015 Category: Hematology Authors: Metzger JM, Tadin-Strapps M, Thankappan A, Strapps WR, Di Poetro M, Leander K, Zhang Z, Shin MK, Levorse J, Desai K, Xu Y, Lai K, Wu W, Chen Z, Cai TQ, Jochnowitz N, Bentley R, Hoos L, Zhou Y, Sepp-Lorenzino L, Seiffert D, Andre P Tags: Thromb Haemost Source Type: research