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. 2009 Jul 13;119(8):2257–2270. doi: 10.1172/JCI35738

Figure 5. GATA- and NFATc-dependent DSCR-1s expression in cultured microvascular endothelial cells.

Figure 5

(A) HMVECs were transiently transfected with DSCR-1–luc2cp; serum starved for 16 hours; incubated for 2 hours with VEGF, LPS, thrombin, or TNF-α; and then assayed for luciferase activity. The results show the mean ± standard deviation of luciferase light units (relative to untreated cells) obtained in triplicate from at least 3 independent experiments. *P < 0.001, **P < 0.05 compared with untreated control. (B) Confluent HMVECs were serum-starved for 16 hours, then treated with VEGF, LPS, thrombin, or TNF-α for 1 hour. Total RNA was harvested and assayed by quantitative real-time PCR using DSCR-1s–specific primers. The results show the mean ± standard deviation of expression levels relative to cyclophilin A obtained in 5 independent experiments. *P < 0.01 compared with untreated control. (C) HMVECs were transfected with 40 nM control siRNA or siRNA against GATA2 and NFATc1, -c2, and -c3 alone or in combination. Transfected cells were treated in the absence or presence of VEGF and assayed for DSCR-1 mRNA by real-time PCR. The results show the mean ± standard deviation of expression levels relative to cyclophilin A obtained in triplicate from 3 independent experiments. *P < 0.001, **P < 0.05 compared with si-Control without VEGF in each experiment. ×2 and ×3, 2-fold molar (80 nM) and 3-fold molar (120 nM) siRNA treatments, respectively.