1991 Fiscal Year Final Research Report Summary
Studies on a novel fibrinolytic mechanism -elastase pathway-
| Project/Area Number |
01570678
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | Kanazawa University, School of Medicine |
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Principal Investigator |
MATSUDA Tamotsu Kanazawa University, School of Medicine, Professor, 医学部, 教授 (30072979)
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| Co-Investigator(Kenkyū-buntansha) |
ASAKURA Hidesaku Kanazawa University, School of Medicine, Assistant, 医学部, 助手 (60192936)
MORISHITA Eriko Kanazawa University, School of Medicine, Assistant, 医学部附属病院, 医員
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| Project Period (FY) |
1989 – 1991
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| Keywords | Leukocyte elastase / Acute promyelocytic leukemia / FDP / D-dimer / Chronic myelocytic leukemia / Thrombomdulin |
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| Research Abstract |
The present study was performed to clarify the role of leukocyte elastase in the abnormalities of coagulation and fibrinolysis. From the study, we showed some findings as follows. (1) The degradation products of leukocyte elastase-treated filbriilogen and fibrin couid be measured by conventional assay method of fibrinogen and/or fibrin degradation products (FDP) using the anti-fibrinogen antibody. (2) We assayed plasma levels of elastase- alpha<aD2. la>D2-proteinase inhibitor complex (E-alpha<_1PI) as the indicator of released leukocyte elasetase in patients with various types of leukimia, and observed marked elevation of E-alpha_1PI levels in patients with acute promyelocytic leukemia (APL) or chronic myelocytic leukemia (CML). (3) The levels of FDP and D-dimer markedly increased in some cases of the APL, whose levels of plasmin-alpha_2-plasmin inhibitor complex (PIC) were within normal limits. This result suggests that leukocyte elastase participates in degradation of fibrnogen and/o
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r fibrin in some cases of APL. (4) Elevated levels of FDP in serum and decreased activities of some clotting factors and inhibitors of blood coagulation were found in patients with CML in chronic phase, although the levels of D-dimer, thrombin-antithrombin III complex and PIC were within normal limits. This finding suggests that leukocyte elastase participates in degradation of somo clotting factors and inhibitors of blood coagulation as well as fibrinogen in this pathological state. (5)We quantitatively assayed plasma levels of thrombomodulin in patients with CML in chronic phase by method of an enzyme-linked immunosorbent assay using a monoclonal antibody to protease-degraded Products of thrombomodulin. Plasma levels of thrombomodulin in CML at diapmosis were significantly increased, and decreased in parallel with decline of WBC counts and E-alpha_1PI levels. Furthermore, a statistically significant correlation was observed between the plasma levels of the thrombomodulin and E-alpha_1PI. These results suggest that leukocyte elastase may split the surface thrombomodulin and release protease degraded fragments of it into the circulation. Less
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