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. 2013 Sep 30;8(9):e75592. doi: 10.1371/journal.pone.0075592

Figure 6. FKHRL1 is essential for relaxin signaling towards iNOS.

Figure 6

Primary rat pulmonary artery endothelial cells (RPAEC, left side) and rat pulmonary artery smooth muscle cells (RPASMC, right side) were processed at baseline, after 90 min hypoxia (5% oxygen), or after another 90 min of normoxia (n = 5 each) in order to determine iNOS activity. Experiments were carried out in the presence of vehicle (control), 5 nM of relaxin, the ERK-1/2 inhibitor PD-98059 (PD) (50 µmol/l), the PI3K inhibitor wortmannin (WM) (100 nM), and combinations thereof. Prior to experiments, cells had been transfected with scrambled siRNA (control), FOXB2 siRNA, or FKHRL1 siRNA. While both transfection with scrambled siRNA and knock-down of non-related forkhead factor, FOXB2, had no influence knock-down of FKHRL-1 abolished the susceptibility of relaxin’s effect towards PI3K inhibition in ischemia and equalized the extent of iNOS induction in reperfusion. P<0.05; *vs. baseline; #vs. relaxin.