ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effect of tissue factor (TF) in extravascular migration of fibrosarcoma cells and hematogenous metastasis.</p><p><b>METHODS</b>The expression of tissue factor in fibrosarcoma HT1080 cells was analyzed by flow cytometry. The extravascular migration of fibrosarcoma cells was observed in a constructed monolayer vascular endothelial cells and extra-cellular matrix model.</p><p><b>RESULT</b>Tissue factor was highly expressed in HT1080 cells. HT1080 migrated and passed through the monolayer vascular endothelial cells to the collagen gel in a time-dependent manner. Anti-TF antibody inhibited extravascular migration of fibrosarcoma cells and the inhibition was concentration-dependent (P<0.05).</p><p><b>CONCLUSION</b>Tissue factor may enhance hematogenous metastasis through extravascular migration of fibrosarcoma cells.</p>
Subject(s)
Humans , Cell Movement , Cells, Cultured , Endothelial Cells , Fibrosarcoma , Metabolism , Pathology , Neoplasm Metastasis , Thromboplastin , Metabolism , PhysiologyABSTRACT
<p><b>OBJECTIVE</b>To evaluate the functional regulation of endothelial Myosin light chain kinase (MLCK) in extravascular migration of fibrosarcoma HT1080 cells.</p><p><b>METHODS</b>An in vitro model of fibrosarcoma cell transmigration across a monolayer of HUVEC cultured on collagen gel was applied to observe extravascular migration of HT1080 cells,and were the electrical resistance of HUVEC monolayer and endothelial MLC phosphorylation in extravascular migration of HT1080 cells.</p><p><b>RESULT</b>HT1080 cells migrated through endothelial cells into collagen gel, the electrical resistance of a HUVEC monolayer was reduced and endothelial MLC phosphorylation was enhanced in extravascular migration of fibrosarcoma cells. Endothelial MLCK inhibitor (ML-7) blocked extravascular migration of HT1080 cells and inhibited reduction of electrical resistance of a HUVEC monolayer and enhancement of endothelial MLC phosphorylation in extravascular migration of HT1080 cells in a dose-dependent manner.</p><p><b>CONCLUSION</b>Endothelial MLCK regulates fibrosarcoma cell transendothelial migration through MLC phosphorylation, leading to cytoskeletal reorganization and endothelial cell constriction, then fibrosarcoma cells migrate into extravascular tissue through the gaps between endothelial cells.</p>
Subject(s)
Humans , Cell Line, Tumor , Cell Movement , Endothelial Cells , Cell Biology , Fibrosarcoma , Pathology , Myosin-Light-Chain Kinase , Metabolism , Physiology , Neoplasm Invasiveness , Umbilical Veins , Cell BiologyABSTRACT
<p><b>OBJECTIVE</b>To study the mechanism of endothelial Rho/Rho kinase in extravascular migration of fibrosarcoma cell.</p><p><b>METHODS</b>We used an in vitro model of fibrosarcoma cell transmigration across a monolayer of human umbilical vein endothelial cell (HUVEC) cultured on collagen gel to observe extravascular migration of fibrosarcoma cells, and then calculated the electrical resistance of HUVEC monolayer and endothelial myosin light chain (MLC) phosphorylation in extravascular migration of fibrosarcoma cells.</p><p><b>RESULTS</b>Fibrosarcoma cells migrated through endothelial cells into collagen gel. The electrical resistance of a HUVEC monolayer reduced and endothelial MLC phosphorylation enhanced in the extravascular migration of fibrosarcoma cells. Endothelial Rho inhibitor (C3 transferase) and Rho kinase inhibitor (Y-27632) inhibited the extravascular migration of fibrosarcoma cells and inhibited the reduction of electrical resistance of a HUVEC monolayer and the enhancement of endothelial MLC phosphorylation in extravascular migration of fibrosarcoma cells.</p><p><b>CONCLUSION</b>Endothelial Rho/Rho kinase may regulate fibrosarcoma cell transendothelial migration through MLC phosphorylation.</p>
Subject(s)
Humans , Amides , Pharmacology , Cell Movement , Physiology , Cells, Cultured , Enzyme Inhibitors , Pharmacology , Fibrosarcoma , Pathology , Human Umbilical Vein Endothelial Cells , Metabolism , Phosphorylation , Pyridines , Pharmacology , rho GTP-Binding Proteins , Metabolism , Physiology , rho-Associated Kinases , Metabolism , PhysiologyABSTRACT
<p><b>OBJECTIVE</b>To study the efficacy of electrolyzed oxidizing water (EOW) and hydrocolloid occlusive dressings in the acceleration of epithelialization in excised burn-wounds in rats.</p><p><b>METHODS</b>Each of the anesthetized Sprague-Dawley rats (n=28) was subjected to a third-degree burn that covered approximately 10% of the total body surface area. Rats were assigned into four groups: Group I (no irrigation), Group II (irrigation with physiologic saline), Group III (irrigation with EOW) and Group IV (hydrocolloid occlusive dressing after EOW irrigation). Wounds were observed macroscopically until complete epithelialization was present, then the epithelialized wounds were examined microscopically.</p><p><b>RESULTS</b>Healing of the burn wounds was the fastest in Group IV treated with hydrocolloid occlusive dressing together with EOW. Although extensive regenerative epidermis was seen in each Group, the proliferations of lymphocytes and macrophages associated with dense collagen deposition were more extensive in Group II, III and IV than in Group I. These findings were particularly evident in Group III and IV.</p><p><b>CONCLUSIONS</b>Wound Healing may be accelerated by applying a hydrocolloid occlusive dressing on burn surfaces after they are cleaned with EOW.</p>