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. Author manuscript; available in PMC: 2013 Sep 9.
Published in final edited form as: Pediatr Res. 2012 Nov 30;73(3):252–262. doi: 10.1038/pr.2012.177

Figure 6.

Figure 6

Figure 6

Figure 6a: Effect of ETA receptor blockade on tube formation in normal and PPHN fetal PAECs. Tube formation was assessed in normal and PPHN PAECs in the presence of ETA receptor blockade (BQ-123 1μM) with and without ET-1 (100nM) treatment. BQ-123 alone had no effect on tube length (data not shown) or number of branch points per HPF in normal and PPHN PAECs. BQ-123 did not prevent the decrease in tube length and number of branch points per HPF with ET-1 treatment. Tube length was decreased by 49% (p<0.01) in normal and 26% (p<0.05) in PPHN PAECs (data not shown) and branch points per HPF by 27% in normal and 34% in PPHN PAECs (p<0.05 for each comaprison).

Figure 6b: Effect of bosentan on tube formation in normal and PPHN fetal PAECs. Tube formation was assessed in normal and PPHN PAECs in the presence of non-selective ETA/ETB receptor blockade (bosentan 1μM) with and without ET-1 (100nM) treatment. Bosentan alone increased tube length by 35% and 42% (p<0.01 for each comparison) in normal and PPHN PAECs respectively (data not shown). Number of branch points per HPF increased by 45% and 62% (p<0.01 for each comparison) in normal and PPHN PAECs respectively. Bosentan prevented the decrease in tube length and number of branch points per HPF with ET-1 treatment. With bosentan and ET-1 treatment in combination, tube length was increased by 42% (p<0.01) in normal and 32% (p<0.05) in PPHN PAECs (data not shown) and branch points per HPF by 48% in normal and 61% in PPHN PAECs (p<0.05 for each comparison).