GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Ovid Technologies (Wolters Kluwer Health)  (3)
  • Chen, Ni  (3)
  • 2015-2019  (3)
Material
Publisher
  • Ovid Technologies (Wolters Kluwer Health)  (3)
Person/Organisation
Language
Years
  • 2015-2019  (3)
Year
  • 1
    Online Resource
    Online Resource
    Abstract 704: Glycation of Vitronectin Inhibits VEGF-induced Angiogenesis by Uncoupling VEGF Receptor-2-αvβ3 Integrin Cross-talk
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 35, No. suppl_1 ( 2015-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. suppl_1 ( 2015-05)
    Abstract: Objective: Glycation of proteins of the vessel wall is thought to play an important role in the pathogenesis of vascular complications in diabetes mellitus. However, no previous study has implicated glycated vitronectin (VN) in controlling vascular endothelial growth factor (VEGF) signaling. Therefore, the goal of this study was to investigate the effects of methylglyoxal (MGO)-glycated VN on VEGF signaling. We tested the hypothesis that glycation of VN down-regulates VEGF receptor-2 (VEGFR-2) activation by uncoupling interaction between VEGFR-2 and αvβ3. Approach and Results: MGO-glycated or unmodified vitronectin were used as substrate for human umbilical vein cells (HUVECs). We studied the effects of glycated VN on VEGF signaling in HUVECs. Glycation of VN inhibited VEGF-induced phosphorylation of VEGFR-2 and intracellular signaling pathway downstream of VEGFR-2. Glycated VN inhibited the binding of VEGFR-2 to β3 integrin and phosphorylation of β3 integrin. LM609 (anti-αvβ3 antibody) inhibited VEGF-induced activation of VEGFR-2 in HUVECs grown on VN. Glycation of VN also significantly decreased VEGF-induced HUVECs migration in vitro and vessel outgrowth in ex vivo angiogenesis model. Conclusions: Glycation of VN inhibits VEGF-induced VEGFR-2 activation by uncoupling VEGFR-2-αvβ3 integrin cross-talk. Glycation of VN causes a reduction in endothelial cells migration and vessel outgrowth. This may provide a mechanism for the failure of collateral sprouting in diabetic microangiopathy.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.35.suppl_1.704
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 1494427-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Abstract 536: Platelet-derived Factor V Promotes Angiogenesis in a Mouse Hindlimb Ischemia Model
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 36, No. suppl_1 ( 2016-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2016-05)
    Abstract: Objective: Coagulation factor V (fV) is distributed in plasma and platelet pools distinguished by physical and functional differences. fV has been extensively studied for its roles in coagulation. The roles of fV in other physiological pathways remain understudied. In the current study, we report that platelet fV is critical for the regulation of angiogenesis in a mouse model of hind-limb ischemia. Methods and Results: Hindlimb ischemia was produced in mice by femoral artery ligation in transgenic mice, with different level of fV gene expression restricted to either the plasma or platelets. The hindlimb blood flow perfusion in mice with higher platelet fV was significantly greater. Furthermore, using a platelet depletion/transfusion procedure, transfusion of platelets with higher level of fV into transgenic mice with undetectable platelet fV significantly rescued the ischemia-mediated impairments in blood flow perfusion. Immunohistochemical analysis also indicated markedly increased capillary formation in ischemic muscle of mice with higher platelet fV. Moreover, thrombin activity was significantly higher in the mice with higher platelet fV. Platelet with higher level of fV demonstrated significantly higher pro-migratory activity in an endothelial cells migration assay. Conclusion: These findings suggest that platelet-derived fV contributes to the control of angiogenesis, in addition to its role in hemostasis. The stimulation is likely associated with thrombin generation due to platelet-derived fV.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.36.suppl_1.536
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 1494427-3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Platelet‐Derived Factor V Is a Critical Mediator of Arterial Thrombosis
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Heart Association Vol. 6, No. 7 ( 2017-07)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 7 ( 2017-07)
    Abstract: Coagulation factor V ( FV ) plays a key role in hemostasis, is present in plasma and platelets, and has both pro‐ and anticoagulant properties; however, the contribution of platelet‐derived FV to arterial thrombosis remains undetermined. Methods and Results Using transgenic mice with various levels of FV gene expression that was restricted to the plasma or platelets, the roles of platelet FV were evaluated in the regulation of arterial thrombosis and platelet activation. Mice with higher levels of platelet FV exhibited faster thrombotic occlusion of the carotid artery after injury compared with mice with lower platelet FV levels. Infusion of platelets with higher levels of FV into transgenic mice with undetectable levels of platelet FV reduced the time to carotid artery occlusion. In contrast, infusion of purified recombinant plasma FV into mice with undetectable platelet FV levels failed to reduce the carotid occlusion times following injury. Evaluation of isolated platelets revealed that platelet‐derived FV was critical for the regulation of platelet activation. These effects were associated with an increased level of expression of P‐selectin and increased cGMP in platelets. Conclusions We established that platelet‐derived FV is a critical mediator of arterial thrombosis that involves platelet activation.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.117.006345
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2653953-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...