Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extraction of leukocytes from dried bloodstains on a variety of surfaces was explored in terms of percentage of recovery. A glycerol-containing solution produced excellent results for many of the surfaces. The outstanding exception was cotton and related cloths, for which a moderate to good result was obtained with a 2-h incubation at 4 degrees C using human serum. A major factor affecting the yield was the blood's ability to form a fibrin network (clotting). In pellets; in blood obtained from a finger prick, a dried crust or pellet yielded only 10 to 25%. A fibrous network containing a large number of entrapped leukocytes was observed under a microscope. This network was identified as fibrin, which acted to collect the cells. The "fibrin-concentrated" leukocytes may be used directly for testing or they can be released by the action of the enzyme plasmin under carefully controlled conditions. Leukocytes may be concentrated from the extraction solution by centrifugation. This step must be done at acidic pH. Leukocyte yields have been high enough to make sex determinations, polymorphic enzyme typing, and human lymphocyte and surface antigen typing feasible in the future.
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PMID:The rehydration and isolation of leukocytes from dried bloodstains. 725 67

The receptor for urokinase-type plasminogen activator (uPA-R) localizes uPA to the cell surface. The receptor-bound uPA converts plasminogen to the trypsin-like endopeptidase plasmin. Thus uPA is involved in the initiation of pericellular proteolysis. Pericellular proteolysis is assumed to facilitate the cellular infiltration into surrounding tissue. The uPA-R has recently been identified as a surface antigen of activated human T lymphocytes. We have characterized the uPA-R of the human CD4 T cell line Jurkat by immunological (flow cytometry), biochemical (ligand blotting), and physico-chemical (Scatchard blotting) methods. The collective data suggest that the human CD4+ T cell line Jurkat expresses a cell surface receptor for uPA similar to that of myelo/monocytes and normal T cells with regard to size, affinity, ligand specificity, and antigenicity. Binding studies using exogenous uPA and subsequent functional assays revealed that receptor-bound uPA retains its enzymatic activity. Saturation of the Jurkat cell uPA-R with exogenous uPA facilitated cellular invasion into fibrin matrices in vitro. uPA-dependent invasion was inhibited in the presence of an anti-catalytic monoclonal anti-uPA antibody. We propose that uPA-R-bound uPA may facilitate the invasiveness of uPA-R-positive T lymphocytes.
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PMID:Urokinase-type plasminogen activator enhances invasion of human T cells (Jurkat) into a fibrin matrix. 791 95

The hepatitis B virus (HBV) is a major cause of human liver disease, including hepatocellular carcinoma (HCC). The prognosis for HCC is largely dependent on the clinicopathological characteristics regarding invasion and metastasis. Enhanced matrix metalloproteinase-9 (MMP-9) expression has been implicated as playing an important role in metastasis and invasion of HCC. However, the relationship between HBV infection and MMP-9 expression in HCC is currently poorly understood. We report here on a study of the levels of MMP-9 and MMP-2 expression in human fetal liver tissue, rat liver tissue, and Chang, HepG2, and Hep3B cells by gelatin zymography. Among these sources, Hep3B cells, which contain the integrated hepatitis B viral genome, continuously secrete the hepatitis B viral surface antigen, and express HBV genomic RNA, expressed high levels of proMMP-9, and a small amount of active MMP-9 was detected in Hep3B cells as assayed by zymography. We investigated the issue of whether HBV infection affects MMP-9 expression, which is known to play an important role in HCC invasion and metastasis. As a first step, human fetal hepatocyte (HFH) and HepG2 (HCC origin, HBV not detected) cells were subjected to infection with HBV, and the resulting infected cells successfully established are hereafter referred to as HFH-T2 and HepG2-HBV. The expression of MMP-9 was upregulated by the infected HBV in HFH-T2 and HepG2-HBV cells, as assayed by zymography, Northern blot, and Western blot analysis, and small amounts of active MMP-9 were detected in HFH-T2 and HepG2-HBV cells as assayed by zymography. The activation of the immature proMMP-9 to the mature MMP-9 could be induced by plasmin treatment. The activation of proMMP-9 was increased to a greater extent with plasmin treatment than without plasmin in HFH-T2 and HepG2-HBV cells but the addition of recombinant TIMP-1 inhibited the activation of proMMP-9. Finally, the addition of plasmin to the invasion assay using Matrigel resulted in an increase in invasiveness of HFH-T2 and HepG2-HBV cells, as well as MMP-9 activation, but the treatment with TIMP-1 inhibited the invasiveness of HFH-T2 and HepG2-HBV cells as well as MMP-9 activation. We conclude from these findings that HBV infection of hepatocytes and HepG2 cells affected the upregulation of MMP-9 expression and MMP-9 activation and, thus, increased the invasion potential by plasmin. To our knowledge, this is a first report showing that an HBV infection is linked to the upregulation of MMP-9 in HCC.
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PMID:Enhanced expression of matrix metalloproteinase-9 by hepatitis B virus infection in liver cells. 1246 65

This retrospective study was carried out to evaluate the seropositivity of hepatitis B surface antigen (HbsAg), anti-hepatitis C virus (HCV), anti-human immunodeficiency virus (HIV) and syphilis in blood donors in Manisa Government Hospital. Data were evaluated in 10,189 blood donors between April 1, 1997, which is the time from which regular records began to be collected, and April 1, 2003. The blood samples of the blood center from April 1, 1997, to January 1, 1998, were examined via the card method, those between January 1, 1998, and January 1, 2002, were examined via micro enzyme-linked immunosorbent assay (ELISA) method and the rest were evaluated with macro ELISA methods. In blood donors, the positivity of HbsAg, anti-HCV anti-HIV and the rapid plasmin reagin test were 2.95%, 0.68%, 0.00% and 0.16%, respectively.
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PMID:Evaluation of hepatitis B surface antigen, anti-hepatitis C virus and anti-human immunodeficiency virus antibodies and syphilis seropositivity in blood donors: six years' seropositivity. 1636 24