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Localization of plasminogen activator inhibitor‐1 production in inflamed appendix by in situ mRNA hybridization
Author(s) -
Whawell Simon A.,
Wang Yiming,
Fleming Kenneth A.,
Thompson Elizabeth M.,
Thompson Jeremy N
Publication year - 1993
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711690111
Subject(s) - in situ hybridization , plasminogen activator , microbiology and biotechnology , appendix , biology , suppression subtractive hybridization , pathology , plasminogen activator inhibitor 1 , peritoneum , t plasminogen activator , immunohistochemistry , mesothelial cell , messenger rna , gene , immunology , medicine , endocrinology , biochemistry , cdna library , paleontology
Abstract The peritoneum has been shown to possess fibrinolytic activity which is thought to play a role in the prevention of intra‐abdominal adhesion formation. Recently inflamed peritoneal tissue has been shown to have reduced fibrinolytic activity secondary to increased levels of plasminogen activator inhibitor‐1 (PAI‐1). The aim of this study was to localize the production of PAI‐1 in appendix tissue using in situ mRNA hybridization. Sections of normal and inflamed appendix were hybridized with a digoxigenin‐labelled cDNA probe. PAI‐1 production was localized to both mcsothelium and serosal blood vessel endothelium in all inflamed appendix samples. Cell identities were confirmed using immunohistochemistry directed against mesothelial and endothlial cell markers. Staining was not seen on sections of normal appendix or on negative control slides of inflamed appendix (hybridization with plasmid DNA, PAI‐1 probe following ribonuclease digestion). The identification of the cells expressing the PAI‐1 gene in peritoneum increases our understanding of the pathophysiological changes in fibrinolytic activity which occur in inflammation and may lead to adhesion formation.