Fig. 4.
Fig. 4. Kinetics of angiostatin-, hTNF-–, and TGF-β1–induced cytotoxicity in BME cells. BME cell monolayers were treated with ehAst, rhAst, or hPlg (left hand column) or with hTNF- or TGF-β1 (right hand column) for 24, 48, or 72 hours at the indicated concentrations. Results are shown as the mean of duplicate samples. Cytotoxicity was assessed using the ethidium homodimer incorporation assay. Although both ehAst and rhAst induce a dose-dependent cytotoxicity in BME cell monolayers (which becomes prominent from 48 hours), sensitivity to the former was greater than to the latter; plasminogen at equimolar concentrations had no effect (240 nmol/L = ∼10 μg/mL for rhAst and ehAst and 22 μg/mL for hPlg). Both hTNF- and TGF-β1 induced dose-dependent cytotoxicity in confluent BME cell monolayers, which became prominent from 48 hours.

Kinetics of angiostatin-, hTNF-–, and TGF-β1–induced cytotoxicity in BME cells. BME cell monolayers were treated with ehAst, rhAst, or hPlg (left hand column) or with hTNF- or TGF-β1 (right hand column) for 24, 48, or 72 hours at the indicated concentrations. Results are shown as the mean of duplicate samples. Cytotoxicity was assessed using the ethidium homodimer incorporation assay. Although both ehAst and rhAst induce a dose-dependent cytotoxicity in BME cell monolayers (which becomes prominent from 48 hours), sensitivity to the former was greater than to the latter; plasminogen at equimolar concentrations had no effect (240 nmol/L = ∼10 μg/mL for rhAst and ehAst and 22 μg/mL for hPlg). Both hTNF- and TGF-β1 induced dose-dependent cytotoxicity in confluent BME cell monolayers, which became prominent from 48 hours.

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