Skip to main content
. 2015 Jan 1;23(1):19–25. doi: 10.4062/biomolther.2014.101

Fig. 3.

Fig. 3.

L-NMMA, NOS inhibitor attenuated hypoxia-inducible VEGF expression. (A) HeLa cells were transfected with pGL2 plasmid of hypoxia response element (HRE)-luciferase (Luc) and incubated under normoxic or hypoxic condition in the presence or absence of L-NMMA. Luc activity was measured with luminometer using Luc substrate. Data in bar graph represent mean ± SED. *p<0.05; **p<0.01, statistical significance vs. normoxia control group. ##p<0.01, statistical significance vs. L-NMMA-untreated group at each time point under hypoxic condition. (B-C) HeLa cells were treated with L-NMMA and incubated under normoxic or hypoxic condition. RNA was purified with TRIZOL reagent. hVEGF and Tβ4 transcript level was measured by RT-PCR (B, top). hVEGF and HIF-1α in cell lysates were detected by western blot analysis (B, bottom). hVEGF transcripts were normalized and data in bar graph represent mean ± SED. *p<0.05, statistical significance vs. normoxia control group. #p<0.05; ##p<0.01, statistical significance vs. L-NMMA-untreated control at each normoxic or hypoxic condition (C).