Figure 3
Figure 3. Erg inhibition increases apoptosis in HUVECs. (A) HUVECs (105) grown on gelatin-coated 6-well plates were transfected with either control GB or Erg-specific GB (100 nM) for 48 hours. Cells were fixed in ethanol and stained with propidium iodide. Sub-G1 apoptotic nuclei were quantified by flow cytometry. Inhibition of Erg increased apoptosis by 3-fold, *P < .05. Values are means plus or minus SEM, n = 3. (B) The regulation of apoptosis by Erg was confirmed by measuring caspase-3 or -7 activity. HUVECs (2 × 103) grown in 96-well microplates were treated with GB as above. After 48 hours, luminescence was measured using the Caspase-3 or -7 Glo Assay (Promega). *P < .05. Values are means plus or minus SEM, n = 4.

Erg inhibition increases apoptosis in HUVECs. (A) HUVECs (105) grown on gelatin-coated 6-well plates were transfected with either control GB or Erg-specific GB (100 nM) for 48 hours. Cells were fixed in ethanol and stained with propidium iodide. Sub-G1 apoptotic nuclei were quantified by flow cytometry. Inhibition of Erg increased apoptosis by 3-fold, *P < .05. Values are means plus or minus SEM, n = 3. (B) The regulation of apoptosis by Erg was confirmed by measuring caspase-3 or -7 activity. HUVECs (2 × 103) grown in 96-well microplates were treated with GB as above. After 48 hours, luminescence was measured using the Caspase-3 or -7 Glo Assay (Promega). *P < .05. Values are means plus or minus SEM, n = 4.

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