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  • 1
    Publikationsdatum: 1995-10-01
    Beschreibung: Fibrin clot retraction may be important in resolution of thrombi and, in platelets, is mediated by integrin alpha IIb beta 3 (GPIIb-IIIa). Nucleated cells that lack alpha IIb beta 3 can retract fibrin clots, and we now report that integrin alpha v beta 3 can support this process. In addition, we compared the capacities of recombinant beta 3 integrins to mediate clot retraction in Chinese hamster ovary and M21 melanoma cells. We found that alpha v beta 3, but not alpha IIb beta 3, could spontaneously support retraction. Transferring the cytoplasmic domain of alpha v to alpha IIb enabled the resulting chimeric alpha IIb beta 3 to support clot retraction. The capacity of the alpha v cytoplasmic domain to support clot retraction was not caused by activation of the ligand binding function of alpha IIb beta 3 or by enhancement of alpha IIb beta 32s capacity to stimulate the formation of focal adhesions or the tyrosine phosphorylation of pp125FAK. These experiments define requirements for alpha IIb beta 3-mediating clot retraction, establish the capacity of alpha v beta 3 to mediate this process, and suggest differing functional roles of the alpha v and alpha IIb cytoplasmic domains.
    Print ISSN: 0006-4971
    Digitale ISSN: 1528-0020
    Thema: Biologie , Medizin
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
    Publikationsdatum: 1995-10-01
    Beschreibung: Fibrin clot retraction may be important in resolution of thrombi and, in platelets, is mediated by integrin alpha IIb beta 3 (GPIIb-IIIa). Nucleated cells that lack alpha IIb beta 3 can retract fibrin clots, and we now report that integrin alpha v beta 3 can support this process. In addition, we compared the capacities of recombinant beta 3 integrins to mediate clot retraction in Chinese hamster ovary and M21 melanoma cells. We found that alpha v beta 3, but not alpha IIb beta 3, could spontaneously support retraction. Transferring the cytoplasmic domain of alpha v to alpha IIb enabled the resulting chimeric alpha IIb beta 3 to support clot retraction. The capacity of the alpha v cytoplasmic domain to support clot retraction was not caused by activation of the ligand binding function of alpha IIb beta 3 or by enhancement of alpha IIb beta 32s capacity to stimulate the formation of focal adhesions or the tyrosine phosphorylation of pp125FAK. These experiments define requirements for alpha IIb beta 3-mediating clot retraction, establish the capacity of alpha v beta 3 to mediate this process, and suggest differing functional roles of the alpha v and alpha IIb cytoplasmic domains.
    Print ISSN: 0006-4971
    Digitale ISSN: 1528-0020
    Thema: Biologie , Medizin
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Publikationsdatum: 2013-11-15
    Beschreibung: Patients with hypercoagulability syndrome can have a wide variety of risk factors that predispose them to develop a thrombotic event. Factor VIII increased levels has been reported as one of these. In this retrospective study we report the frequency of increased levels of factor VIII activity found in patients referred for hypercoagulability assessment to our reference center. Material and methods Review of clinical and laboratory database of patients referred for hypercoagulability assessment. Results are presented as percentages. Results Of 323 patients with hypercoagulability syndrome, 98 (30.3%) had increased levels of Factor VIII activity, male-female ratio 1:1.8, mean age 49.8 ± 15 y-o. Sixty (61.2%) patients had a venous thrombotic event and 73.3% of them had recurrence. Ten (10.2%) had an arterial thrombotic event and 23 a combined arterial and venous thrombosis with recurrent episodes of 70.0 and 82.6% respectively. Five patients had no clotting events. Thrombosis in unusual sites was found in 22 patients. Conclusion Increased levels of Factor VIII activity are found in 30.3 % of patients with hypercoagulability syndromes, almost two thirds develop a venous thrombotic event and recurrences occur in 75.3%. Disclosures: No relevant conflicts of interest to declare.
    Print ISSN: 0006-4971
    Digitale ISSN: 1528-0020
    Thema: Biologie , Medizin
    Standort Signatur Erwartet Verfügbarkeit
    BibTip Andere fanden auch interessant ...
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