Sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by immunoblot analysis of plasma thrombomodulin concentrate revealed that four degraded forms of thrombomodulin with different molecular weights are present in plasma. Plasma concentrations of thrombomodulin in patients with various diseases were measured by two methods of enzyme- linked immunosorbent assay using monoclonal antibodies. One method measures intact thrombomodulin and degraded forms of thrombomodulin; the other does not detect the two smaller degraded forms of thrombomodulin present in plasma. The results indicated that thrombomodulin was increased in the circulating blood of patients with disseminated intravascular coagulation syndrome, pulmonary thromboembolism, adult respiratory distress syndrome, chronic renal failure, or acute hepatic failure. The different values obtained by the two methods indicate that the increase of plasma thrombomodulin found in these patients was mainly due to an increase of the smaller fragments of degraded forms, suggesting that the release of thrombomodulin from endothelial cells was accelerated in various disease states by proteolytic activity generated on the surface of the endothelium and may be removed from the circulation mostly by the kidneys and liver.
Thrombomodulin, a thrombin receptor on the vascular endothelial cell surface, is released into circulating blood. The plasma concentrations in patients with collagen vascular diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis, juvenile rheumatoid arthritis, Sjögren's syndrome, systemic sclerosis, polymyositis and/or dermatomyositis (PM/DM), Behçet's disease, and Wegener's granulomatosis, were measured and compared with those of healthy persons. The mean plasma thrombomodulin concentrations in patients with juvenile rheumatoid arthritis, systemic sclerosis, PM/DM, Wegener's granulomatosis, and active states of SLE, rheumatoid arthritis, and Beçhet's disease were significantly higher than those in the control group. Patients with Wegener's granulomatosis showed the highest mean value. The mean values in patients with inactive states of the diseases and Sjögren's syndrome were not significantly different from the values in the control group. In cases of juvenile rheumatoid arthritis, systemic sclerosis, PM/DM, and Wegener's granulomatosis, patients with active interstitial pneumonitis or extensive pulmonary lesions frequently showed higher values of plasma thrombomodulin than those without overt pulmonary involvement. Elevated plasma thrombomodulin values were decreased along with amelioration of the diseases by treatment. These results may indicate that plasma thrombomodulin measurement may be helpful for evaluating vascular injury in patients with collagen diseases.
Sodium dodecyl sulfate-polyacrylamide gel electrophoresis followed by immunoblot analysis of plasma thrombomodulin concentrate revealed that four degraded forms of thrombomodulin with different molecular weights are present in plasma. Plasma concentrations of thrombomodulin in patients with various diseases were measured by two methods of enzyme- linked immunosorbent assay using monoclonal antibodies. One method measures intact thrombomodulin and degraded forms of thrombomodulin; the other does not detect the two smaller degraded forms of thrombomodulin present in plasma. The results indicated that thrombomodulin was increased in the circulating blood of patients with disseminated intravascular coagulation syndrome, pulmonary thromboembolism, adult respiratory distress syndrome, chronic renal failure, or acute hepatic failure. The different values obtained by the two methods indicate that the increase of plasma thrombomodulin found in these patients was mainly due to an increase of the smaller fragments of degraded forms, suggesting that the release of thrombomodulin from endothelial cells was accelerated in various disease states by proteolytic activity generated on the surface of the endothelium and may be removed from the circulation mostly by the kidneys and liver.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.