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  • 1
    Online Resource
    Online Resource
    Notch promotes vascular maturation by inducing integrin-mediated smooth muscle cell adhesion to the endothelial basement membrane
    American Society of Hematology ; 2012
    In:  Blood Vol. 119, No. 9 ( 2012-03-01), p. 2149-2158
    Details
    In: Blood, American Society of Hematology, Vol. 119, No. 9 ( 2012-03-01), p. 2149-2158
    Abstract: Vascular development and angiogenesis initially depend on endothelial tip cell invasion, which is followed by a series of maturation steps, including lumen formation and recruitment of perivascular cells. Notch ligands expressed on the endothelium and their cognate receptors expressed on perivascular cells are involved in blood vessel maturation, though little is known regarding the Notchdependent effectors that facilitate perivascular coverage of nascent vessels. Here, we report that vascular smooth muscle cell (VSMC) recognition of the Notch ligand Jagged1 on endothelial cells leads to expression of integrin αvβ3 on VSMCs. Once expressed, integrin αvβ3 facilitates VSMC adhesion to VWF in the endothelial basement membrane of developing retinal arteries, leading to vessel maturation. Genetic or pharmacologic disruption of Jagged1, Notch, αvβ3, or VWF suppresses VSMC coverage of nascent vessels and arterial maturation during vascular development. Therefore, we define a Notch-mediated interaction between the developing endothelium and VSMCs leading to adhesion of VSMCs to the endothelial basement membrane and arterial maturation.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2011-04-348706
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2012
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
    Online Resource
    Online Resource
    Molecular Imaging Reveals Rapid Reduction of Endothelial Activation in Early Atherosclerosis With Apocynin Independent of Antioxidative Properties
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 33, No. 9 ( 2013-09), p. 2187-2192
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 9 ( 2013-09), p. 2187-2192
    Abstract: Antioxidative drugs continue to be developed for the treatment of atherosclerosis. Apocynin is an nicotinamide adenine dinucleotide phosphate oxidase inhibitor with anti-inflammatory properties. We used contrast-enhanced ultrasound molecular imaging to assess whether short-term apocynin therapy in atherosclerosis reduces vascular oxidative stress and endothelial activation Approach and Results— Genetically modified mice with early atherosclerosis were studied at baseline and after 7 days of therapy with apocynin (4 mg/kg per day IP) or saline. Contrast-enhanced ultrasound molecular imaging of the aorta was performed with microbubbles targeted to vascular cell adhesion molecule 1 (VCAM-1; MB V ), to platelet glycoprotein Ibα (MB Pl ), and control microbubbles (MB Ctr ). Aortic vascular cell adhesion molecule 1 was measured using Western blot. Aortic reactive oxygen species generation was measured using a lucigenin assay. Hydroethidine oxidation was used to assess aortic superoxide generation. Baseline signal for MB V (1.3±0.3 AU) and MB Pl (1.5±0.5 AU) was higher than for MB Ctr (0.5±0.2 AU; P 〈 0.01). In saline-treated animals, signal did not significantly change for any microbubble agent, whereas short-term apocynin significantly ( P 〈 0.05) reduced vascular cell adhesion molecule 1 and platelet signal (MB V : 0.3±0.1; MB Pl : 0.4±0.1; MB Ctr : 0.3±0.2 AU; P =0.6 between agents). Apocynin reduced aortic vascular cell adhesion molecule 1 expression by 50% ( P 〈 0.05). However, apocynin therapy did not reduce reactive oxygen species content, superoxide generation, or macrophage content. Conclusions— Short-term treatment with apocynin in atherosclerosis reduces endothelial cell adhesion molecule expression. This change in endothelial phenotype can be detected by molecular imaging before any measurable decrease in macrophage content and is not associated with a detectable change in oxidative burden.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.113.301710
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1494427-3
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  • 3
    Online Resource
    Online Resource
    Signaling-mediated cooperativity between glycoprotein Ib-IX and protease-activated receptors in thrombin-induced platelet activation
    American Society of Hematology ; 2016
    In:  Blood Vol. 127, No. 5 ( 2016-02-04), p. 626-636
    Details
    In: Blood, American Society of Hematology, Vol. 127, No. 5 ( 2016-02-04), p. 626-636
    Abstract: GPIb-IX signaling cooperates with PAR signaling to promote platelet response to low concentrations of thrombin, which are important in vivo. Thrombin induces a GPIb-IX–specific signaling pathway that requires the cytoplasmic domain of GPIbα, 14-3-3 protein, Rac1, and LIMK1.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2015-04-638387
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2016
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
    Online Resource
    Online Resource
    Biomechanical Properties of Bonds Mediated by the von Willebrand Factor A1 Domain during Platelet Adhesion under Flow Conditions.
    American Society of Hematology ; 2004
    In:  Blood Vol. 104, No. 11 ( 2004-11-16), p. 3665-3665
    Details
    In: Blood, American Society of Hematology, Vol. 104, No. 11 ( 2004-11-16), p. 3665-3665
    Abstract: The initial attachment of platelets to vascular lesions exposed to a high wall shear rate (γw) depends on the interaction between the membrane glycoprotein (GP) Ibα, a component of the GP Ib-IX-V receptor complex, and the A1 domain of surface-immobilized von Willebrand factor (VWFA1). We performed perfusion experiments under different flow conditions to measure transient platelet contacts onto immobilized recombinant VWFA1 and determine the probability of bond formation (capturing) and resistance to tensile stress (bond lifetime) of VWFA1-GP Ibα interactions. To define how molecular conformations influence the biomechanical properties of the bonds, we compared fragments exhibiting the native dimeric assembly of A1 domain with monomeric fragments obtained by selective purification of recombinant protein expressed in stable D. melanogaster cell lines. The minimum coating concentration of dimeric VWFA1 at which platelet adhesion events were statistically significantly different from nonspecific interactions on uncoated glass was 1 μg/ml. In the range of γw between 30 and 30,000 s−1, there was no threshold value for the initiation of adhesion, as seen for selectins. The number of adhering platelets first increased and then decreased with monotonically increasing γw, indicating the effect of transport phenomena as well as hydrodynamic forces on the VWFA1-GP Ibα interaction. Maximum event number was at 5,000 s−1 for dimeric and 1,500 s−1 for monomeric VWFA1. The platelet count had no statistically relevant influence on the efficiency of capturing and duration of adhesive contacts. As γw increased, a higher coating concentration of the VWF A1 domain was required to initiate platelet adhesion. The coating concentration determined the number of individual adhesion events that could occur over a defined period of time but did not affect the residence time, which is a measure of the strength of the bond between the receptor and the ligand. Hydrodynamic forces generated by blood flow shortened the duration of VWF-GP Ibα interactions. The percentage of platelets that had a residence time of less than 0.1 s increased almost linearly with increasing γw. Dimeric A1 domain was more efficient than the monomeric counterpart in promoting platelet adhesion as it displayed activity at lower coating concentrations. At permissible γw, a 10-fold higher monomer than dimer coating concentration (2 vs. 20 μg/ml) was required to obtain a similar capturing efficiency. Moreover, the upper limit of γw compatible with the initiation of adhesion was significantly higher for dimeric as compared to monomeric A1 domain. Doubling the dimer coating concentration resulted in a 5-fold increase in the γw limit for adhesion, but the same increase in the monomer coating concentration did not enhance the probability of bond formation at higher γw. In spite of the substantial difference in capturing efficiency, monomeric and dimeric VWFA1 supported platelet adhesion events of similar duration at any given γw, indicating that a different molecular conformation did not affect the lifetime of the interaction with GP Ibα. These results indicate that the dimeric assembly of A1 domains in VWF multimers may be crucial to support the initiation of platelet adhesion at high shear rates, but the duration of each adhesion event is limited by intrinsic properties of the individual VWFA1-GP Ibα bond.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V104.11.3665.3665
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2004
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 5
    Online Resource
    Online Resource
    Increased thrombogenesis and embolus formation in mice lacking glycoprotein V
    American Society of Hematology ; 2001
    In:  Blood Vol. 98, No. 2 ( 2001-07-15), p. 368-373
    Details
    In: Blood, American Society of Hematology, Vol. 98, No. 2 ( 2001-07-15), p. 368-373
    Abstract: The glycoprotein (GP) Ib-V-IX complex plays a critical role in initiating platelet adhesion to von Willebrand factor (vWF) at the site of vascular injury. The complex also forms a high-affinity binding site for thrombin. Using an intravital microscopy mouse model, it was previously established that vWF plays a critical role in mediating platelet adhesion and thrombus formation following mesenteric arteriolar injury induced by ferric chloride. Further characterization of this model showed that these thrombotic events were also thrombin dependent. Using this vWF- and thrombin-dependent model, this study shows that GP V gene deficiency significantly accelerates both platelet adhesion and thrombus formation in mice following arteriolar injury. The time required for vessel occlusion in GP V–deficient (GP V−/−) mice was significantly shorter than that in wild-type mice. Interestingly, large emboli were also produced in GP V−/− mice, but not in wild-type mice, causing frequent downstream occlusion. However, when the 2 genotypes were compared in the in vitro perfusion chamber where thrombin was inhibited by heparin, no significant differences were found in either initial single-platelet adhesion or thrombus volume. These results demonstrate that GP V−/− mice have accelerated thrombus growth in response to vascular injury and suggest that this is caused by enhanced thrombin-induced platelet activation rather than enhanced binding of GPIb-V-IX to vWF. Absence of GP V also compromises thrombus stability.
    Type of Medium: Online Resource
    ISSN: 1528-0020 , 0006-4971
    URL: Article
    DOI: 10.1182/blood.V98.2.368
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2001
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 6
    Online Resource
    Online Resource
    Lymphocytic choriomeningitis virus Clone 13 infection causes either persistence or acute death dependent on IFN-1, cytotoxic T lymphocytes (CTLs), and host genetics
    Proceedings of the National Academy of Sciences ; 2018
    In:  Proceedings of the National Academy of Sciences Vol. 115, No. 33 ( 2018-08-14)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 115, No. 33 ( 2018-08-14)
    Abstract: Understanding of T cell exhaustion and successful therapy to restore T cell function was first described using Clone (Cl) 13 variant selected from the lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) 53b parental strain. T cell exhaustion plays a pivotal role in both persistent infections and cancers of mice and humans. C57BL/6, BALB, SWR/J, A/J, 129, C3H, and all but one collaborative cross (CC) mouse strain following Cl 13 infection have immunosuppressed T cell responses, high PD-1, and viral titers leading to persistent infection and normal life spans. In contrast, the profile of FVB/N, NZB, PL/J, SL/J, and CC NZO mice challenged with Cl 13 is a robust T cell response, high titers of virus, PD-1, and Lag3 markers on T cells. These mice all die 7 to 9 d after Cl 13 infection. Death is due to enhanced pulmonary endothelial vascular permeability, pulmonary edema, collapse of alveolar air spaces, and respiratory failure. Pathogenesis involves abundant levels of Cl 13 receptor alpha-dystroglycan on endothelial cells, with high viral replication in such cells leading to immunopathologic injury. Death is aborted by blockade of interferon-1 (IFN-1) signaling or deletion of CD8 T cells.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1804674115
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2018
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Integrin activation controls metastasis in human breast cancer
    Proceedings of the National Academy of Sciences ; 2001
    In:  Proceedings of the National Academy of Sciences Vol. 98, No. 4 ( 2001-02-13), p. 1853-1858
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 98, No. 4 ( 2001-02-13), p. 1853-1858
    Abstract: Metastasis is the primary cause of death in human breast cancer. Metastasis to bone, lungs, liver, and brain involves dissemination of breast cancer cells via the bloodstream and requires adhesion within the vasculature. Blood cell adhesion within the vasculature depends on integrins, a family of transmembrane adhesion receptors, and is regulated by integrin activation. Here we show that integrin αvβ3 supports breast cancer cell attachment under blood flow conditions in an activation-dependent manner. Integrin αvβ3 was found in two distinct functional states in human breast cancer cells. The activated, but not the nonactivated, state supported tumor cell arrest during blood flow through interaction with platelets. Importantly, activated αvβ3 was expressed by freshly isolated metastatic human breast cancer cells and variants of the MDA-MB 435 human breast cancer cell line, derived from mammary fat pad tumors or distant metastases in severe combined immunodeficient mice. Expression of constitutively activated mutant αvβ3 D723R , but not αvβ3 WT , in MDA-MB 435 cells strongly promoted metastasis in the mouse model. Thus breast cancer cells can exhibit a platelet-interactive and metastatic phenotype that is controlled by the activation of integrin αvβ3. Consequently, alterations within tumors that lead to the aberrant control of integrin activation are expected to adversely affect the course of human breast cancer.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.98.4.1853
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2001
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Apolipoprotein A-IV binds αIIbβ3 integrin and inhibits thrombosis
    Springer Science and Business Media LLC ; 2018
    In:  Nature Communications Vol. 9, No. 1 ( 2018-09-06)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 9, No. 1 ( 2018-09-06)
    Abstract: Platelet αIIbβ3 integrin and its ligands are essential for thrombosis and hemostasis, and play key roles in myocardial infarction and stroke. Here we show that apolipoprotein A-IV (apoA-IV) can be isolated from human blood plasma using platelet β3 integrin-coated beads. Binding of apoA-IV to platelets requires activation of αIIbβ3 integrin, and the direct apoA-IV-αIIbβ3 interaction can be detected using a single-molecule Biomembrane Force Probe. We identify that aspartic acids 5 and 13 at the N-terminus of apoA-IV are required for binding to αIIbβ3 integrin, which is additionally modulated by apoA-IV C-terminus via intra-molecular interactions. ApoA-IV inhibits platelet aggregation and postprandial platelet hyperactivity. Human apoA-IV plasma levels show a circadian rhythm that negatively correlates with platelet aggregation and cardiovascular events. Thus, we identify apoA-IV as a novel ligand of αIIbβ3 integrin and an endogenous inhibitor of thrombosis, establishing a link between lipoprotein metabolism and cardiovascular diseases.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-018-05806-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2553671-0
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  • 9
    Online Resource
    Online Resource
    Apolipoprotein A-IV is an Endogenous Protective Factor for Atherothrombosis
    Elsevier BV ; 2018
    In:  Atherosclerosis Supplements Vol. 32 ( 2018-06), p. 30-31
    Details
    In: Atherosclerosis Supplements, Elsevier BV, Vol. 32 ( 2018-06), p. 30-31
    Type of Medium: Online Resource
    ISSN: 1567-5688
    URL: Article
    DOI: 10.1016/j.atherosclerosissup.2018.04.087
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 1499887-7
    detail.hit.zdb_id: 2098677-4
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  • 10
    Online Resource
    Online Resource
    Inflammatory platelet production stimulated by tyrosyl-tRNA synthetase mimicking viral infection
    Proceedings of the National Academy of Sciences ; 2022
    In:  Proceedings of the National Academy of Sciences Vol. 119, No. 48 ( 2022-11-29)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 119, No. 48 ( 2022-11-29)
    Abstract: Platelets play a role not only in hemostasis and thrombosis, but also in inflammation and innate immunity. We previously reported that an activated form of tyrosyl-tRNA synthetase (YRS ACT ) has an extratranslational activity that enhances megakaryopoiesis and platelet production in mice. Here, we report that YRS ACT mimics inflammatory stress inducing a unique megakaryocyte (MK) population with stem cell (Sca1) and myeloid (F4/80) markers through a mechanism dependent on Toll-like receptor (TLR) activation and type I interferon (IFN-I) signaling. This mimicry of inflammatory stress by YRS ACT was studied in mice infected by lymphocytic choriomeningitis virus (LCMV). Using Sca1/EGFP transgenic mice, we demonstrated that IFN-I induced by YRS ACT or LCMV infection suppressed normal hematopoiesis while activating an alternative pathway of thrombopoiesis. Platelets of inflammatory origin (Sca1/EGFP + ) were a relevant proportion of those circulating during recovery from thrombocytopenia. Analysis of these “inflammatory” MKs and platelets suggested their origin in myeloid/MK-biased hematopoietic stem cells (HSCs) that bypassed the classical MK-erythroid progenitor (MEP) pathway to replenish platelets and promote recovery from thrombocytopenia. Notably, inflammatory platelets displayed enhanced agonist-induced activation and procoagulant activities. Moreover, myeloid/MK-biased progenitors and MKs were mobilized from the bone marrow, as evidenced by their presence in the lung microvasculature within fibrin-containing microthrombi. Our results define the function of YRS ACT in platelet generation and contribute to elucidate platelet alterations in number and function during viral infection.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2212659119
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2022
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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