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Condition: Thrombosis

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Total 185 results found since Jan 2013.

Prolyl-4-Hydroxylase 2 Potentially Contributes to Hepatocellular Carcinoma-Associated Erythrocytosis by Maintaining Hepatocyte Nuclear Factor-4α Expression
Conclusion: Our findings show that PHD2 represents a potential contributing factor for HCC-associated erythrocytosis. Selective inhibition of PHD2 in HCC cells might be considered as a new way to manage erythrocytosis in HCC patients.Cell Physiol Biochem 2015;37:2257-2264
Source: Cellular Physiology and Biochemistry - December 1, 2015 Category: Cytology Source Type: research

Factor XII full and partial null in rat confers robust antithrombotic efficacy with no bleeding
This report aims at exploring quantitatively the relationship between FXII inhibition and thromboprotection. FXII full and partial null in rats were established via zinc finger nuclease-mediated knockout and siRNA-mediated knockdown, respectively. The rats were subsequently characterized in thrombosis and hemostasis models. Knockout rats exhibited complete thromboprotection in both the arteriovenous shunt model (∼100% clot weight reduction) and the FeCl3-induced arterial thrombosis model (no reduction in blood flow), without any increase in cuticle bleeding time compared with wild-type control rats. Ex-vivo aPTT and the ...
Source: Blood Coagulation and Fibrinolysis - October 31, 2015 Category: Hematology Tags: Original Articles Source Type: research

Novel hydroxybutyl chitosan nanoparticles for siRNA delivery targeting tissue factor inhibits proliferation and induces apoptosis in human vascular smooth muscle cells.
Authors: Wan K, Li J, Li D, Ge J, Wang Y, Li X, Guo Y, Guo J, Leng M, Wang P, An Y Abstract Chitosan, a polysaccharide isolated from shrimp and other crustacean shells, has been widely investigated for DNA and siRNA delivery. Despite substantial effort having been made to improve chitosan as a non‑viral gene delivery vector, the application is severely limited by its poor solubility under physiological conditions. Hydroxybutyl chitosan (HBC), a modified chitosan, is soluble under neutral conditions. Tissue factor (TF) is involved in the pathogenesis of cardiovascular diseases by promoting thrombus formation and i...
Source: Molecular Medicine Reports - October 28, 2015 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Thrombin-induced IL-8/CXCL8 release is mediated by CK2, MSK1, and NF-κB pathways in Human lung epithelial cells.
In this study, we further investigated the role of casein kinase 2 (CK2)/mitogen stress-activated protein kinase 1 (MSK1)-dependent p65 phosphorylation in thrombin-induced NF-κB activation and IL-8/CXCL8 release. Thrombin-induced IL-8/CXCL8 release was inhibited by CK2 inhibitors (apigenin and tetrabromobenzotriazole, TBB), small interfering RNA of CK2β (CK2β siRNA), and MSK1 siRNA. Treatment of cells with thrombin caused increases in CK2β phosphorylation at Ser209, which was inhibited by a protein kinase C α (PKCα) inhibitor (Ro-32-0432). Thrombin-induced MSK1 phosphorylation at Ser581 and Akt phosphorylation at Ser...
Source: European Journal of Pharmacology - October 10, 2015 Category: Drugs & Pharmacology Authors: Lin CH, Shih CH, Chen BC Tags: Eur J Pharmacol Source Type: research

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

Estrogen-Related Receptor γ Plays a Key Role in Vascular Calcification Through the Upregulation of BMP2 Expression.
CONCLUSIONS: The present results indicate that ERRγ plays a key role in vascular calcification by upregulating the BMP2 signaling pathway, suggesting that inhibition of ERRγ is a potential therapeutic strategy for the prevention of vascular calcification. PMID: 26404484 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - September 24, 2015 Category: Cardiology Authors: Kim JH, Choi YK, Do JY, Choi YK, Ha CM, Lee SJ, Jeon JH, Lee WK, Choi HS, Park KG, Lee IK Tags: Arterioscler Thromb Vasc Biol Source Type: research

Endothelial Nitric Oxide Synthase-Derived Nitric Oxide Prevents Dihydrofolate Reductase Degradation via Promoting S-Nitrosylation.
CONCLUSIONS: We conclude that S-nitrosylation of DHFR at cysteine 7 by eNOS-derived NO is crucial for DHFR stability. We also conclude that NO-induced stabilization of DHFR prevents eNOS uncoupling via regeneration of tetrahydrobiopterin, an essential eNOS cofactor. PMID: 26381869 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - September 17, 2015 Category: Cardiology Authors: Cai Z, Lu Q, Ding Y, Wang Q, Xiao L, Song P, Zou MH Tags: Arterioscler Thromb Vasc Biol 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

High-Density Lipoproteins Reduce Endothelial-to-Mesenchymal Transition.
CONCLUSIONS: We provide the first in vitro evidence that the endothelial-protective and antifibrotic effects of HDL include the reduction in endothelial-to-mesenchymal transition. PMID: 26088574 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - June 18, 2015 Category: Cardiology Authors: Spillmann F, Miteva K, Pieske B, Tschöpe C, Van Linthout S Tags: Arterioscler Thromb Vasc Biol 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

UFM1 Protects Macrophages from oxLDL-Induced Foam Cell Formation Through a Liver X Receptor α Dependent Pathway.
CONCLUSIONS: Taken together, our results showed that UFM1 could suppress foam cell formation via the LXRα-dependent pathway. PMID: 26040753 [PubMed - as supplied by publisher]
Source: Journal of Atherosclerosis and Thrombosis - June 5, 2015 Category: Cardiology Tags: J Atheroscler Thromb Source Type: research

Eicosapentaenoic Acid Prevents Saturated Fatty Acid-Induced Vascular Endothelial Dysfunction: Involvement of Long-Chain Acyl-CoA Synthetase.
CONCLUSIONS: These results suggest that the ACSL, p21, and NF-κB-dependent pathway may possibly be involved in PA-induced vascular endothelial dysfunction, and that EPA ameliorates this at least in part through the regulation of ACSL3 expression. PMID: 26016511 [PubMed - as supplied by publisher]
Source: Journal of Atherosclerosis and Thrombosis - May 31, 2015 Category: Cardiology Tags: J Atheroscler Thromb Source Type: research

Reduction of Mitochondria-Endoplasmic Reticulum Interactions by Acetylcholine Protects Human Umbilical Vein Endothelial Cells From Hypoxia/Reoxygenation Injury.
CONCLUSIONS: Our data suggest that ER-mitochondria interplay plays an important role in reperfusion injury in the endothelium and may be a novel molecular target for endothelial protection. Acetylcholine attenuates both intracellular and mitochondrial Ca(2+) overload and protects endothelial cells from H/R injury, presumably by disrupting the ER-mitochondria interaction. PMID: 25977565 [PubMed - as supplied by publisher]
Source: Arteriosclerosis, Thrombosis and Vascular Biology - May 14, 2015 Category: Cardiology Authors: He X, Bi XY, Lu XZ, Zhao M, Yu XJ, Sun L, Xu M, Wier WG, Zang WJ Tags: Arterioscler Thromb Vasc Biol Source Type: research