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Hui Zhou, Meihong Deng, Yingjie Liu, Chenxuan Yang, Rosemary Hoffman, Jingjiao Zhou, Patricia A Loughran, Melanie J Scott, Matthew D Neal, Timothy R Billiar
Thrombocytopenia impairs host defense and hemostasis in sepsis. However, the mechanisms of how platelets regulate host defense are not fully understood. High-mobility group box 1 (HMGB1), a danger-associated molecular pattern protein, is released during infection and contributes to the pathogenesis of sepsis. Platelets express HMGB1, which is released on activation and has been shown to play a critical role in thrombosis, monocyte recruitment, and neutrophil extracellular trap (NET) production. However, the contribution of platelet HMGB1 to host defense is unknown...
March 27, 2018: Blood Advances
Valeryi K Lishko, Valentin P Yakubenko, Tatiana P Ugarova, Nataly P Podolnikova
Platelet Factor 4 (PF4) is one of the most abundant cationic proteins secreted from α-granules of activated platelets. Based on its structure, PF4 was assigned to the CXC family of chemokines and has been shown to have numerous effects on myeloid leukocytes. However, the receptor for PF4 remains unknown. Here, we demonstrate that PF4 induces leukocyte responses through the integrin Mac-1 (αM β2 , CD11b/CD18). Human neutrophils, monocytes, U937 monocytic and HEK293 cells expressing Mac-1 strongly adhered to immobilized PF4 in a concentration-dependent manner...
March 14, 2018: Journal of Biological Chemistry
Sonali Vadi, Vishal Peshattiwar
Fondaparinux, a pentasaccharide administered for heparin-induced thrombocytopenia (HIT), can lead to the occurrence of thrombocytopenia. This patient underwent aortic stent graft placement for Salmonella paratyphi A-infected abdominal aortic aneurysm. Fondaparinux was administered for anticoagulation that led to a dramatic decline in his platelet counts. Investigations revealed HIT profile, PF4/heparin by particle gel immunoassay to be positive. Fondaparinux, a prescribed anticoagulant for HIT can paradoxically predispose to thrombocytopenia...
February 2018: Indian Journal of Critical Care Medicine
Huina Zhang, Fan Yang, Yichen Guo, Li Wang, Fang Fang, Hao Wu, Shaoping Nie, Yifan Wang, Man-Lung Fung, Yu Huang, Haiteng Deng, Yanwen Qin, Xinliang Ma, Yongxiang Wei
OBJECTIVE: Obstructive sleep apnea hypopnea syndrome (OSAHS) is an independent risk factor for many clinical complications. However, how OSAHS cause multiple organ injury and initiate inter-organ communication remains unclear. Moreover, despite it is well-recognized that chronic intermittent hypoxia (CIH) is a main feature of OSAHS, specific contribution of CIH to overall OSAHS-initiated pathological complications remains unclear. This study aimed to use an unbiased proteomic approach to determine whether OSAHS alters protein profiles of serum extracellular microvesicles (SEMVs) and how CIH contributes to such alterations...
March 6, 2018: Metabolism: Clinical and Experimental
Frédéric Adam, Alexandre Kauskot, Mathieu Kurowska, Nicolas Goudin, Isabelle Munoz, Jean-Claude Bordet, Jian-Dong Huang, Marijke Bryckaert, Alain Fischer, Delphine Borgel, Geneviève de Saint Basile, Olivier D Christophe, Gaël Ménasché
OBJECTIVE: Platelet secretion is crucial for many physiological platelet responses. Even though several regulators of the fusion machinery for secretory granule exocytosis have been identified in platelets, the underlying mechanisms are not yet fully characterized. APPROACH AND RESULTS: By studying a mouse model (cKO [conditional knockout]Kif5b ) lacking Kif5b (kinesin-1 heavy chain) in its megakaryocytes and platelets, we evidenced unstable hemostasis characterized by an increase of blood loss associated to a marked tendency to rebleed in a tail-clip assay and thrombus instability in an in vivo thrombosis model...
March 8, 2018: Arteriosclerosis, Thrombosis, and Vascular Biology
Benfang Wang, Jianjiang Yu, Ting Wang, Ying Shen, Dandan Lin, Xin Xu, Yiqiang Wang
AIMS: To define the possible effect of diabetic conditions on megakaryocytes, the long-know precursors of platelets and lately characterized modulator of hematopoietic stem quiescence-activation transition. METHODS: Megakaryoblastic MEG-01 cell culture and TPO/SCF/IL-3-induced differentiation of human umbilical blood mononuclear cells toward megakaryocytes were used to test effects of glycated bovine serum albumin (BSA-AGEs). The ob/ob mice and streptozotocin-treated mice were used as models of hyperglycemia...
February 8, 2018: Acta Diabetologica
Shengnan Wang, Junshu Jiang, Yue Wang, Qilan Jia, Shufang Dai, Yuping Wang, Li Lv, Jihong Wang
Recombinant Lampetra japonica RGD-peptide (rLj-RGD3), a soluble protein containing three RGD sequences, was acquired from the oral salivary glands of Lampetra japonica using recombinant DNA technology. The aim of this study was to investigate the protective effects of rLj-RGD3 against acute myocardial infarction (AMI) induced by coronary artery thrombosis, as well as the underlying mechanisms. A rat model of AMI caused by ferric chloride-induced thrombosis on the surface of the left anterior descending (LAD) coronary artery was successfully established...
February 3, 2018: Biochemical and Biophysical Research Communications
R Palankar, T P Kohler, K Krauel, J Wesche, S Hammerschmidt, A Greinacher
BACKGROUND: Activated platelets release the chemokine platelet factor 4 (PF4) stored in their granules. PF4 binds to polyanions (P) on bacteria, undergoes a conformational change and exposes neoepitopes. These neoepitopes induce production of anti-PF4/P antibodies. As PF4 binds to a variety of bacteria, anti-PF4/P IgG can bind and opsonize several bacterial species. OBJECTIVE: Here we investigated whether platelets are able to kill bacteria directly after recognizing anti-PF4/P IgG opsonized bacteria in the presence of PF4 via their FcγRIIA...
January 19, 2018: Journal of Thrombosis and Haemostasis: JTH
Theodore E Warkentin, Donald M Arnold, John G Kelton, Jo-Ann I Sheppard, James W Smith, Ishac Nazy
BACKGROUND: HIT is a prothrombotic drug reaction caused by platelet-activating antibodies that recognize PF4/heparin complexes. It is unknown whether platelet-activating antibodies are detectable at the onset of the HIT-related platelet count fall. METHODS: Available blood samples from 18 patients obtained at onset of HIT were tested using the serotonin-release assay (SRA), a test for platelet-activating antibodies, and a PF4-dependent ELISA. Patient samples showing a delay of >2 days between ELISA and SRA seroconversion were tested for subthreshold levels of platelet-activating antibodies using two modifications of the SRA that amplify detection of HIT antibodies...
January 8, 2018: Chest
Grace M Lee, Manali Joglekar, Maragatha Kuchibhatla, Sanjay Khandelwal, Rui Qi, Lubica Rauova, Gowthami M Arepally
Anti-protamine (PRT)/heparin antibodies are a newly described class of heparin-dependent antibodies occurring in patients exposed to PRT and heparin during cardiac surgery. To understand the biologic significance of anti-PRT/heparin antibodies, we developed a murine monoclonal antibody (ADA) specific for PRT/heparin complexes and compared it to patient-derived anti-PRT/heparin antibodies, as well as comparing polyclonal and monoclonal antibodies with anti-platelet factor 4 (PF4)/heparin. Using monoclonal antibodies and polyclonal patient-derived antibodies, we show distinctive binding patterns of anti-PRT/heparin antibodies as compared with PF4/heparin antibodies...
April 25, 2017: Blood Advances
Siti Norasikin Mohd Nafi, Fauziah Idris, Hasnan Jaafar
Background: Angiogenic activity has been considered to reflect important molecular events during breast tumour development. The present study concerned cellular and molecular changes of MNU-induced breast tumours subjected to promotion and suppression of angiogenesis. Methods: Female Sprague Dawley rats at the age of 21 days received MNU at the dose 70 mg/kg of body weight by intraperitoneal injection. Three months post-carcinogen initiation, mammary tumours were palpated and their growth was monitored. When the tumour diameter reached 1...
December 28, 2017: Asian Pacific Journal of Cancer Prevention: APJCP
Xuefeng Li, Yu Liang, Zhili Qiao, Jiaoxia Yang, Pengfei Han, Binghai Zhao, Fengxiang Li, Hengjuan Lv, Jifang Guo, Fengmin Gao, Li Li
The aim of this study was to explore how atrial natriuretic polypeptide (ANP) affects the properties and function of endothelial cells. Gene expression data GSE56976 generated at 0, 1, and 6 hours after ANP incubation in human umbilical vein endothelial cells (HUVEC) was used. Microarray data were preprocessed for differentially expressed genes (DEGs) in each time-dependent group. Next, gene ontology (GO), pathway analysis, and transcriptional regulation were performed. Co-expression clustering analysis of DEGs and functional enrichment analysis of co-expression modules were processed...
December 27, 2017: International Heart Journal
Marion Mussbacher, Waltraud C Schrottmaier, Manuel Salzmann, Christine Brostjan, Johannes A Schmid, Patrick Starlinger, Alice Assinger
Platelets store a plethora of different molecules within their granules, modulating numerous pathways, not only in coagulation, but also in angiogenesis, wound healing, and inflammatory diseases. These molecules get rapidly released upon activation and therefore represent an easily accessible indirect marker for platelet activation. Accurate analysis of platelet-derived molecules in the plasma requires appropriate anticoagulation to avoid in vitro activation and subsequent degranulation of platelets, potentially causing artificially high levels and masking biologically relevant differences within translational research studies...
2017: PloS One
Feng-Ming Spring Kong, Lujun Zhao, Luhua Wang, Yuhchyau Chen, Jie Hu, Xiaolong Fu, Chunxue Bai, Li Wang, Theodore S Lawrence, Mitchell S Anscher, Adam Dicker, Paul Okunieff
Background: Sample quality is critical for biomarker detection in oncology, and platelet degradation and contamination in plasma have a remarkable impact on the ability to accurately quantify many blood-based biomarkers. Platelet factor 4 (PF4) can be used as an indicator to monitor sample quality. This multicenter study aimed to determine the impact of critical components of the blood sample handling process on platelet degradation/contamination and to establish an optimal method for collecting platelet-poor plasma samples...
December 2017: Translational Lung Cancer Research
Nesreen Z Alsmadi, Sarah J Shapiro, Christopher S Lewis, Vinit M Sheth, Trevor A Snyder, David W Schmidtke
Due to the critical roles that platelets play in thrombosis during many biological and pathological events, altered platelet function may be a key contributor to altered hemostasis, leading to both thrombotic and hemorrhagic complications. Platelet adhesion at arterial shear rates occurs through binding to von Willebrand Factor via the glycoprotein (GP) GPIb receptor. GPIb binding can induce platelet activation distinguishable by P-selectin (CD62P) surface expression and αIIb β3 activation, resulting in platelet aggregation and formation of the primary hemostatic plug to stop bleeding...
November 2017: Biomicrofluidics
Constantinos Bakogiannis, Marco Sachse, Kimon Stamatelopoulos, Konstantinos Stellos
Platelets are inflammatory anuclear cells with a well-established role in the development and manifestation of atherosclerosis. Activated platelets secrete a plethora of chemokines including CXCL4 or platelet factor 4 (PF4), CCL5, CXCL12 or stromal cell derived factor-1α (SDF-1α), CXCL16 and others, which initiate or promote local inflammatory processes at sites of vascular injury. These processes are mainly mediated by the recruitment of circulating haematopoietic stem cells, neutrophils, monocytes or lymphocytes on vascular wall...
December 1, 2017: Cytokine
Ming Y Lim, Joyce Foster, Angela Rourk, Charles S Greenberg
Many medical centers are faced with a major challenge in making an accurate diagnosis of heparin-induced thrombocytopenia (HIT) and ensuring appropriate changes in management strategy in line with guideline recommendations. We report the initial and long-term impact and challenges of institution-wide changes in the diagnosis and management of HIT in the inpatient setting at an academic medical center. We established a HIT Task Force, consisting of a multidisciplinary team of non-malignant hematologists, nursing, pharmacist, pathology, blood bank and clinical lab informatics...
January 2018: Journal of Thrombosis and Thrombolysis
Ivana Markovic, Zeljko Debeljak, Bojana Bosnjak, Maja Marijanovic
Heparin induced thrombocytopenia (HIT) is a life-threatening disorder which diagnosis depends on laboratory evaluation. The objective of this report is to present the impact of different laboratory methods for HIT detection on the diagnostic evaluation process. In this case, a 78-year old female patient previously diagnosed with monoclonal gammopathy of undetermined significance (MGUS) was administered with heparin for pulmonary embolism treatment. Patient's initial diagnostic work-up (determination of platelet count and prothrombin time measurement for monitoring of pharmacotherapy) was followed by the clinical estimation of HIT likelihood by "4Ts" score, two immunoassays (ID-PaGIA Heparin/PF4 Antibody Test and ELISA PF4 IgG assay) and one functional test called high-performance liquid chromatography serotonin release assay (HPLC-SRA)...
October 15, 2017: Biochemia Medica: časopis Hrvatskoga Društva Medicinskih Biokemičara
Angela Huynh, Donald M Arnold, Jane C Moore, James W Smith, John G Kelton, Ishac Nazy
Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction characterized by IgG antibodies bound to complexes of platelet factor 4 (PF4) and heparin. The majority of diagnostic tests for HIT rely on an exogenous source of PF4 to identify anti-PF4/heparin antibodies. These include the PF4-dependent enhanced serotonin release assay (PF4-SRA) among others. Using a bacterial expression system, we developed a novel and efficient method of producing recombinant human PF4 (rhPF4) that is biochemically and antigenically similar to platelet-derived human PF4...
November 27, 2017: Platelets
Emmanuel J Favaloro
Heparin induced thrombocytopenia (HIT) is a potentially fatal condition that arises subsequent to formation of antibodies against complexes containing heparin, usually platelet-factor 4-heparin ("anti-PF4-heparin"). Assessment for HIT involves both clinical evaluation and, if indicated, laboratory testing for confirmation or exclusion, typically using an initial immunological assay ("screening"), and only if positive, a secondary functional assay for confirmation. Many different immunological and functional assays have been developed...
February 2018: American Journal of Hematology
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