Relaxin Protects Rat Lungs from Ischemia-Reperfusion Injury via Inducible NO Synthase: Role of ERK-1/2, PI3K, and Forkhead Transcription Factor FKHRL1
Figure 5
Relaxin, via PI3K, phosphorylates FKHRL-1.
Isolated rat lungs perfused with buffer in recirculatory mode were processed at baseline, after 90(n = 6 each) in order to determine protein expression (panel A) and Ser-253 phosphorylation (panel B) of the forkhead transcription factor, FKHRL1. 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. (A) Representative Western blot from lung homogenates produced after ischemia. (B) Quantification of Western blot data (n = 6 per group). Relaxin causes FKHRL-1 phosphorylation during ischemia in a PI3K (wortmannin)-dependent fashion; there is no dependence of ERK-1/2. P<0.05; *vs. baseline; #vs. relaxin.