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  1. Book ; Conference proceedings: Proceedings of the 7th Symposium on Hemostasis - Old System, New Players, New Directions

    Pawlinski, Rafal

    [May 15 - 17, 2014, Chapel Hill, North Carolina]

    (Thrombosis research ; 133, Suppl. 1)

    2014  

    Event/congress Symposium on Hemostasis - Old System, New Players, New Directions (2014, ChapelHillNC)
    Author's details guest ed.: Rafal Pawlinski
    Series title Thrombosis research ; 133, Suppl. 1
    Collection
    Language English
    Size S59 S. : Ill.
    Publisher Elsevier
    Publishing place Amsterdam u.a.
    Publishing country Netherlands
    Document type Book ; Conference proceedings
    HBZ-ID HT018273389
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Zs A 863 -133,Suppl.1- not available for loan Zeitschriften-Lesesaal

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  2. Article ; Online: Cut me if you can!

    Pawlinski, Rafal

    Blood

    2018  Volume 131, Issue 11, Page(s) 1155–1156

    MeSH term(s) Humans ; Protein C ; Receptor, PAR-1 ; Sepsis ; Stroke
    Chemical Substances Protein C ; Receptor, PAR-1
    Language English
    Publishing date 2018-02-09
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-02-829564
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Platelet HMGB1: the venous clot coordinator.

    Pawlinski, Rafal

    Blood

    2016  Volume 128, Issue 20, Page(s) 2376–2378

    MeSH term(s) Blood Coagulation ; Blood Platelets ; HMGB1 Protein ; Humans ; Platelet Aggregation ; Thrombosis ; Veins
    Chemical Substances HMGB1 Protein
    Language English
    Publishing date 2016-11-16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2016-09-738740
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: It's "PT" for SCD!

    Pawlinski, Rafal

    Blood

    2015  Volume 126, Issue 15, Page(s) 1739–1740

    Abstract: In this issue of Blood, Arumugam et al report that long-term reduction of prothrombin (PT) expression results in diminished vascular inflammation, attenuation of multiple organ damage, and survival advantage in a mouse model of sickle cell disease (SCD). ...

    Abstract In this issue of Blood, Arumugam et al report that long-term reduction of prothrombin (PT) expression results in diminished vascular inflammation, attenuation of multiple organ damage, and survival advantage in a mouse model of sickle cell disease (SCD).
    MeSH term(s) Anemia, Sickle Cell/complications ; Animals ; Genetic Therapy ; Hypertension, Pulmonary/prevention & control ; Inflammation/prevention & control ; Male ; Prothrombin/physiology ; Vascular Diseases/prevention & control
    Chemical Substances Prothrombin (9001-26-7)
    Language English
    Publishing date 2015-10-07
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2015-08-666594
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Inhibit the calpain to climb the mountain.

    Pawlinski, Rafal

    Blood

    2014  Volume 123, Issue 8, Page(s) 1123–1124

    MeSH term(s) Animals ; Blood Platelets/metabolism ; Calpain/metabolism ; Humans ; Hypoxia/metabolism ; Male ; Thrombosis/metabolism
    Chemical Substances Calpain (EC 3.4.22.-) ; Capns1 protein, rat (EC 3.4.22.-) ; CAPNS1 protein, human (EC 3.4.22.52)
    Language English
    Publishing date 2014-02-20
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2013-12-543397
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Biased agonism of protease-activated receptor-1 regulates thrombo-inflammation in murine sickle cell disease.

    Ramadas, Nirupama / Lowder, Kailyn / Dutton, Joshua / Trebak, Fatima / Faes, Camille / Griffin, John H / Pawlinski, Rafal / Mosnier, Laurent O / Sparkenbaugh, Erica M

    Blood advances

    2024  

    Abstract: Sickle cell disease (SCD) is a hereditary hemoglobinopathy marked by hemolytic anemia and vaso-occlusive events (VOE). Chronic endothelial activation, inflammation, and coagulation activation contribute to vascular congestion, VOE, and end-organ damage. ... ...

    Abstract Sickle cell disease (SCD) is a hereditary hemoglobinopathy marked by hemolytic anemia and vaso-occlusive events (VOE). Chronic endothelial activation, inflammation, and coagulation activation contribute to vascular congestion, VOE, and end-organ damage. Coagulation proteases like thrombin and activated protein C (APC) modulate inflammation and endothelial dysfunction by activating protease-activated receptor 1 (PAR1), a G-protein coupled receptor. Thrombin cleaves PAR1 at Arg41, while APC cleaves PAR1 at Arg46, initiating either pro-inflammatory or cytoprotective signaling, respectively, a signaling conundrum known as biased agonism. Our prior research established the role of thrombin and PAR1 in vascular stasis in an SCD mouse model. However, the role of APC and APC-biased PAR1 signaling in thrombin generation, inflammation and endothelial activation in SCD remains unexplored. Inhibition of APC in SCD mice increased thrombin generation, inflammation, and endothelial activation during both steady state and TNFα challenge. To dissect the individual contributions of thrombin-PAR1 and APC-PAR1 signaling, we employed transgenic mice with point mutations at two PAR1 cleavage sites, ArgR41Gln (R41Q) imparting insensitivity to thrombin and Arg46Gln (R46Q) imparting insensitivity to APC. Sickle bone marrow chimeras expressing PAR1-R41Q exhibited reduced thrombo-inflammatory responses compared to PAR1-WT or PAR1-R46Q mice. These findings highlight the potential benefit of reducing thrombin-dependent PAR1 activation while preserving APC-PAR1 signaling in SCD thromboinflammation. These results also suggest that pharmacological strategies promoting biased PAR1 signaling could effectively mitigate vascular complications associated with SCD.
    Language English
    Publishing date 2024-04-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2023011907
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Pathologically stiff erythrocytes impede contraction of blood clots: Comment.

    Ilich, Anton / Sparkenbaugh, Erica M / Wolberg, Alisa S / Key, Nigel S / Pawlinski, Rafal

    Journal of thrombosis and haemostasis : JTH

    2021  Volume 19, Issue 11, Page(s) 2893–2894

    MeSH term(s) Erythrocytes ; Humans ; Thrombosis
    Language English
    Publishing date 2021-10-28
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 2112661-6
    ISSN 1538-7836 ; 1538-7933
    ISSN (online) 1538-7836
    ISSN 1538-7933
    DOI 10.1111/jth.15512
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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  8. Article ; Online: Plasma kallikrein supports FXII-independent thrombin generation in mouse whole blood.

    Wan, Jun / Dhrolia, Sophia / Kasthuri, Rohan R / Prokopenko, Yuriy / Ilich, Anton / Saha, Prakash / Roest, Mark / Wolberg, Alisa S / Key, Nigel S / Pawlinski, Rafal / Bendapudi, Pavan K / Mackman, Nigel / Grover, Steven P

    Blood advances

    2024  

    Abstract: Plasma kallikrein (PKa) is an important activator of factor (F)XII of the contact pathway of coagulation. Several studies have shown that PKa also possesses procoagulant activity independent of FXII, likely through its ability to directly activate FIX. ... ...

    Abstract Plasma kallikrein (PKa) is an important activator of factor (F)XII of the contact pathway of coagulation. Several studies have shown that PKa also possesses procoagulant activity independent of FXII, likely through its ability to directly activate FIX. We evaluated the procoagulant activity of PKa using a mouse whole blood (WB) thrombin generation (TG) assay. TG was measured in WB from PKa-deficient mice using contact pathway or extrinsic pathway triggers. PKa-deficient WB had significantly reduced contact pathway-initiated TG compared to wild-type controls and was comparable to that observed in FXII-deficient WB. PKa-deficient WB supported equivalent extrinsic pathway-initiated TG compared to wild-type controls. Consistent with the presence of FXII-independent functions of PKa, targeted blockade of PKa with either small molecule or antibody-based inhibitors significantly reduced contact pathway-initiated TG in FXII-deficient WB. Inhibition of activated FXII (FXIIa) using an antibody-based inhibitor significantly reduced TG in PKa-deficient WB, consistent with a PKa-independent function of FXIIa. Experiments using mice expressing low levels of tissue factor demonstrated that persistent TG present in PKa- and FXIIa-inhibited WB was driven primarily by endogenous tissue factor. Our work demonstrates that PKa contributes significantly to contact pathway-initiated TG in the complex milieu of mouse WB and that a component of this contribution occurs in a FXII-independent manner.
    Language English
    Publishing date 2024-04-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2024012613
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: A novel mouse whole blood thrombin generation assay sensitive to FXI- and FIX-mediated amplification of coagulation.

    Wan, Jun / Tanratana, Pansakorn / Roest, Mark / Gruber, Andras / Pawlinski, Rafal / Wolberg, Alisa S / Mackman, Nigel / Grover, Steven P

    Blood advances

    2023  Volume 7, Issue 9, Page(s) 1915–1925

    Abstract: Thrombin generation (TG) assays serve as a valuable tool to study the amplifying roles of intrinsic pathway factors in human coagulation and provide functional insights into the increased bleeding observed in individuals deficient in factors (F) XI, IX, ... ...

    Abstract Thrombin generation (TG) assays serve as a valuable tool to study the amplifying roles of intrinsic pathway factors in human coagulation and provide functional insights into the increased bleeding observed in individuals deficient in factors (F) XI, IX, or VIII. Mice are used extensively in hemostasis research owing to the availability of coagulation factor-deficient mice. However, phenotypic differences between mouse and human TG have become apparent. In this study, we describe a novel, calibrated mouse whole blood (WB) TG assay used to assess the amplifying roles of intrinsic pathway factors in mouse coagulation. WB- and plasma-TG was triggered with either silica or tissue factor (TF) in samples from wild-type mice and mice deficient for FXII, FXI, or FIX. Expectedly, silica-triggered WB-TG and platelet-poor plasma (PPP)-TG were significantly reduced by deficiencies for FXII, FXI, or FIX. FXII deficiency had no effect on WB-TG or PPP-TG when triggered with TF. However, FXI deficiency resulted in significantly reduced WB-TG triggered by low concentrations of TF but had no effect on TF-triggered PPP-TG. FIX deficiency profoundly reduced WB-TG when triggered by low or high concentrations of TF whereas TG in PPP or platelet-rich plasma was only moderately reduced under these conditions. In conclusion, we have developed a novel mouse WB-TG assay with enhanced sensitivity to FXI- and FIX-dependent amplification of coagulation compared with an established plasma-TG assay. The enhanced sensitivity of WB-TG to FXI and FIX-dependent amplification of coagulation suggests an important role of blood cells in this process.
    MeSH term(s) Animals ; Humans ; Mice ; Blood Coagulation ; Hemorrhage ; Hemostasis ; Thrombin/metabolism ; Thromboplastin/metabolism ; Factor XI/metabolism ; Factor IX/metabolism
    Chemical Substances Thrombin (EC 3.4.21.5) ; Thromboplastin (9035-58-9) ; Factor XI (9013-55-2) ; Factor IX (9001-28-9)
    Language English
    Publishing date 2023-01-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2022008720
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Hypercoagulable state in sickle cell disease.

    Faes, Camille / Sparkenbaugh, Erica M / Pawlinski, Rafal

    Clinical hemorheology and microcirculation

    2018  Volume 68, Issue 2-3, Page(s) 301–318

    Abstract: Chronic activation of coagulation is one of the features of sickle cell disease (SCD). Increased tissue factor expression, phosphatidylserine exposure, thrombin generation and fibrinolysis, as well as decreased levels of natural anticoagulants have been ... ...

    Abstract Chronic activation of coagulation is one of the features of sickle cell disease (SCD). Increased tissue factor expression, phosphatidylserine exposure, thrombin generation and fibrinolysis, as well as decreased levels of natural anticoagulants have been reported in SCD patients and in the mouse models of SCD. Consistent with this, patients with SCD are prone to develop thrombotic complications. In addition, the altered morphology of sickle red blood cells (RBC) may also alter the properties and dynamics of clot formation in SCD patients. Clinical data and results from animal models have revealed complex interactions between coagulation, chronic hemolysis, and inflammation suggesting that activation of coagulation may contribute to the pathophysiology of SCD.
    MeSH term(s) Anemia, Sickle Cell/blood ; Animals ; Blood Coagulation Tests/methods ; Erythrocytes/metabolism ; Humans ; Mice ; Mice, Transgenic
    Language English
    Publishing date 2018
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1381750-4
    ISSN 1875-8622 ; 1386-0291
    ISSN (online) 1875-8622
    ISSN 1386-0291
    DOI 10.3233/CH-189013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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