Fig. 2.
Fig. 2. Analysis of DAF, CD59, and MCP expression on DMECs and HUVECs following stimulation with cytokines. Monolayers of ECs were incubated for 48 hours in the presence or absence of IL-1β (10 ng/mL), IFNγ (500 U/mL), TNF- (10 ng/mL), or TNF- and IFN-γ before harvesting and analysis by flow cytometry. DAF, CD59, and MCP were detected using MoAbs 5B2, A35, and TRA-2-10, respectively. The results (mean ± SD) are expressed as the RFI (MFI of test sample divided by MFI of irrelevant isotype-matched negative control) for (A, B) DAF, (C, D) CD59, and (E, F) MCP. The results are representative of 4 experiments performed on different EC lines. *P < .05, **P < .02. The efficacy of cytokines used in each experiment was confirmed by their ability to induce VCAM-1 or ICAM-1 as appropriate (data not shown). US, unstimulated.

Analysis of DAF, CD59, and MCP expression on DMECs and HUVECs following stimulation with cytokines. Monolayers of ECs were incubated for 48 hours in the presence or absence of IL-1β (10 ng/mL), IFNγ (500 U/mL), TNF- (10 ng/mL), or TNF- and IFN-γ before harvesting and analysis by flow cytometry. DAF, CD59, and MCP were detected using MoAbs 5B2, A35, and TRA-2-10, respectively. The results (mean ± SD) are expressed as the RFI (MFI of test sample divided by MFI of irrelevant isotype-matched negative control) for (A, B) DAF, (C, D) CD59, and (E, F) MCP. The results are representative of 4 experiments performed on different EC lines. *P < .05, **P < .02. The efficacy of cytokines used in each experiment was confirmed by their ability to induce VCAM-1 or ICAM-1 as appropriate (data not shown). US, unstimulated.

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