Determination of α2-antiplasmin-plasmin complex in human plasma with an enzyme-linked immunosorbent assay

Pelzer, H.; Pilgrim, Adeiye; Schwarz, Angela; Merte, D.; Keuper, H.; Hock, Hans

doi:10.1016/0268-9499(93)90025-q

Cited by 30 publications

(30 citation statements)

References 13 publications

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“…29,30 We measured the TAT concentration in the 3 cohorts of mice after anti-GPIX antibody treatment by ELISA assay. At resting state, TULA-2 −/− or TULA-2 +/− mice did not show a significant difference in TAT levels compared with TULA-2 +/+ mice.…”

Section: Tula-2 Reduction Potentiates Hit-like Thrombocytopenia and Tmentioning

confidence: 99%

TULA-2 (T-Cell Ubiquitin Ligand-2) Inhibits the Platelet Fc Receptor for IgG IIA (FcγRIIA) Signaling Pathway and Heparin-Induced Thrombocytopenia in Mice

Zhou

Abraham

Renna

et al. 2016

ATVB

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Objective-The objective of this study is to investigate the role of T-cell ubiquitin ligand-2 (TULA-2) in the platelet Fc receptor for IgG IIA (FcγRIIA) pathway and in the pathogenesis of heparin-induced thrombocytopenia (HIT). Approach and Results-HIT is a life-threatening thrombotic disease in which IgG antibodies against the heparin-platelet factor 4 complex activate platelets via FcγRIIA. We reported previously differential expression of TULA-2 in human population was linked to FcγRIIA responsiveness. In this study, we investigated the role of TULA-2, a protein phosphatase, in the FcγRIIA pathway and HIT pathogenesis by crossing TULA-2 −/− mice with transgenic FcγRIIA +/+ mice. Ablation of TULA-2 resulted in hyperphosphorylation of spleen tyrosine kinase, linker for the activation of T cells, and phospholipase Cγ2 in platelets via FcγRIIA activation. Platelet integrin activation, granule secretion, phosphatidylserine exposure, and aggregation were also enhanced in TULA-2 −/− murine platelets. Compared with wild-type mice, TULA-2 −/− mice showed aggravated antibody-mediated thrombocytopenia, augmented thrombin generation, and shortened tail bleeding time. In contrast, there was no significant difference between TULA-2 −/− and TULA-2 +/+ platelets in platelet spreading and clot retraction. Of note, heterozygous TULA-2 +/− mice, whose platelets contained 50% as much protein as the TULA-2 +/+ platelets, showed significantly increased platelet reactivity and more severe thrombocytopenia in vivo compared with TULA-2 +/+ mice. Conclusions-Together, the data demonstrate that not only the absence of TULA-2 but also the relative level of TULA-2 expression modulates FcγRIIA-mediated platelet reactivity and HIT in vivo. TULA-2 expression could be a valuable marker for HIT and inhibiting TULA-2 may serve as a potential therapy to reverse the bleeding adverse effect of anticoagulants.

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Section: Tula-2 Reduction Potentiates Hit-like Thrombocytopenia and Tmentioning

confidence: 99%

TULA-2 (T-Cell Ubiquitin Ligand-2) Inhibits the Platelet Fc Receptor for IgG IIA (FcγRIIA) Signaling Pathway and Heparin-Induced Thrombocytopenia in Mice

Zhou

Abraham

Renna

et al. 2016

ATVB

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“…The Japanese criteria are based on a scoring system based on the presence of underlying disease, bleeding, organ failure, and the results of global coagulation tests [fibrinogen, fibrin degradation products (FDP), platelet count, and prothrombin time (PT)]. Hemostatic molecular markers, such as D-dimer [7], soluble fibrin (SF) [8], thrombin-antithrombin complex (TAT) [9], plasmin-plasmin inhibitor complex (PPIC) [10], and thrombomodulin [11], can be also measured. However, the latter markers are very sensitive but not specific for DIC, and they cannot be measured in all hospitals.…”

Section: Introductionmentioning

confidence: 99%

Comparison of diagnostic criteria for disseminated intravascular coagulation (DIC): diagnostic criteria of the International Society of Thrombosis and Hemostasis (ISTH) and of the Japanese Ministry of Health and Welfare for overt DIC

et al. 2003

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We compared the criteria set by the International Society of Thrombosis and Hemostasis (ISTH) for the diagnosis of disseminated intravascular coagulation (DIC) with the criteria of the Japanese Ministry of Health and Welfare (JMHW) set for the diagnosis of overt DIC. We studied 1,284 Japanese patients with DIC. The rate of agreement in the diagnosis of DIC by the two diagnostic systems was 67.4%. In addition, only 2.0% of non-DIC patients by JMHW criteria were diagnosed with overt DIC by ISTH criteria, suggesting that ISTH for overt DIC includes typical cases of DIC. The concordance of diagnosis for DIC by ISTH and JMHW was significantly high in patients with trauma or acute promyelocytic leukemia. About 70% of DIC or overt DIC patients had more than 1 point in the scoring system for prothrombin time, but >50% of those patients had 0 point for plasma fibrinogen level. Abnormal fibrin and fibrinogen degradation product (FDP) levels and platelet counts were observed in >88% of DIC and overt DIC patients but were observed in >50% of non-DIC patients, indicating that these parameters are sensitive markers but not specific markers for the diagnosis of DIC. Considered together, our results suggest that the diagnostic criteria for DIC and overt DIC could be improved by changing the cut-off values of the global coagulation tests. Am. J. Hematol. 74:17-22, 2003.

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“…The inhibition complex (inactive proteinase/inhibitor complex) can be measured quantitatively by enzyme immunoassay. 41 There is a significant correlation between elevated concentrations of the thrombin/antithrombin III complex (TAT) and thrombotic events, eg, in patients with septic shock. 42 After pretreatment of the rats with saline, LPS, or LTA (2 to 24 hours, nϭ3 or 4), a blood sample was centrifuged to obtain plasma, and the concentration of TAT was determined by using the Enzygnost TAT microimmunoassay (Behringwerke AG).…”

Section: Measurement Of Plasma Levels Of Tat In the Ratmentioning

confidence: 99%

Lipoteichoic Acid Induces Delayed Protection in the Rat Heart

Zacharowski

Frank

Otto

et al. 2000

ATVB

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Abstract-Classic ischemic preconditioning transiently (30 to 120 minutes) protects the myocardium against subsequent lethal ischemia/reperfusion injury. After dissipation of this acute protection, a second window of protection (SWOP) appears 12 to 24 hours later; this SWOP lasts up to 3 days. Several triggers induce a SWOP, including brief repetitive cycles of coronary artery occlusion, rapid ventricular pacing, stimulation of adenosine A 1 receptors, and administration of wall fragments of Gram-negative bacteria, such as lipopolysaccharide (LPS). The aim of this study was to investigate whether lipoteichoic acid (LTA), a cell wall fragment of Gram-positive bacteria, can induce a SWOP in a rat model of left anterior descending coronary artery (LAD) occlusion (25 minutes) and reperfusion (2 hours). Thus, 166 male Wistar rats were pretreated (2 to 24 hours) with saline, LTA (1 mg/kg IP), or LPS (1 mg/kg IP) and subjected to LAD occlusion/reperfusion. Pretreatment with LTA or LPS for 16 hours led to a substantial, Ϸ65%, reduction in infarct size and a reduction in the release of cardiac troponin T into the plasma. The dose of LTA used had no toxic effect (on any of the parameters studied), whereas the same dose of LPS caused a time-dependent activation of the coagulation system and liver injury. By use of RNase protection assays, it was determined that LPS caused a time-dependent induction of tumor necrosis factor-␣, interleukin-1␤, and manganese superoxide dismutase mRNA content in the heart, whereas LTA failed to induce manganese superoxide dismutase. LPS also caused an upregulation of the expression of intercellular adhesion molecule-1 and P-selectin, whereas LTA downregulated these molecules and attenuated the accumulation of polymorphonuclear granulocytes caused by myocardial ischemia/reperfusion. This study demonstrates for the first time that pretreatment with LTA at 8 to 24 hours before myocardial ischemia significantly reduces (1) infarct size, (2) cardiac troponin T, and (3) the histological signs of tissue injury in rats subjected to LAD occlusion and reperfusion. The mechanism(s) underlying the observed cardioprotective effects of LTA warrants further investigation but is likely to be related to its ability to inhibit the interactions between the coronary vascular endothelium and polymorphonuclear granulocytes. Therefore, LTA represents a novel and promising agent capable of enhancing myocardial tolerance to ischemia/reperfusion injury. Key Words: lipopolysaccharide Ⅲ lipoteichoic acid Ⅲ myocardial infarct size Ⅲ delayed preconditioning Ⅲ myocardial ischemia D uring coronary artery angioplasty or open heart surgery, regional or global iatrogenic cardiac ischemia is a common event. Reperfusion of previously ischemic myocardium leads to ischemia/reperfusion injury with enhanced propagation of arrhythmias, 1 stunning, 2 and cardiomyocyte cell death. 3 Over the last few years, the population of patients with coronary artery disease undergoing coronary artery angioplasty or bypass surgery has increased, as h...

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Determination of α2-antiplasmin-plasmin complex in human plasma with an enzyme-linked immunosorbent assay

Cited by 30 publications

References 13 publications

TULA-2 (T-Cell Ubiquitin Ligand-2) Inhibits the Platelet Fc Receptor for IgG IIA (FcγRIIA) Signaling Pathway and Heparin-Induced Thrombocytopenia in Mice

TULA-2 (T-Cell Ubiquitin Ligand-2) Inhibits the Platelet Fc Receptor for IgG IIA (FcγRIIA) Signaling Pathway and Heparin-Induced Thrombocytopenia in Mice

Comparison of diagnostic criteria for disseminated intravascular coagulation (DIC): diagnostic criteria of the International Society of Thrombosis and Hemostasis (ISTH) and of the Japanese Ministry of Health and Welfare for overt DIC

Lipoteichoic Acid Induces Delayed Protection in the Rat Heart

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