Pediatric Critical Care Medicine:

May 2014 - Volume 15 - Issue 4_suppl - p 112

doi: 10.1097/01.pcc.0000449217.13842.9d

REGULATION MECHANISM OF MAP KINASES ON AQUAPORIN 5 MRNA AND PROTEIN EXPRESSSIONS IN HYPEROXIC LUNG INJURY

Xu, F.

ABSTRACT

Background and aims: Long-term oxygen exposure can result in actue lung injury.

Aims: To investigate regulation mechanism of mitogen activated protein kinases (MAPKs) signaling pathway on Aquaporin 5 (AQP5) expression disorder in hyperoxic lung injury (HLI).

Methods: Forty-eight Wistar rats aged three weeks old were randomly divided into 8 groups (n=6), i.e., room-air group (A), hyperoxia group (H), hyperoxia + inhibitor groups (the ERK inhibitor PD 98059, the p38 inhibitor SB 203580, he JNK inhibitor SP 600125),and air+ inhibitors groups (A+PD98059/SB203580/SP600125). AQP5 protein expression in lung tissue was detected by Western blot analysis. AQP5 mRNA expression was determined by real-time fluorescent quantitative polymerase chain reaction method.

Results: Lung injury developed in hyperoxia exposure groups. The protein level of AQP5 was down-regulated in H group and H+ inhibitors groups (H+PD98059/SB203580/SP600125) than that in A group, but AQP5 protein expressiowere markedly higher in H+SB203580 and H+SP600125 groups compared with that of H group (P<0.05), and this change was more significant in H+SB203580 group (P<0.05).There was no difference in AQP5 protein level between H group and H+PD203580 group. The mRNA level of AQP5 changed similarly to AQP5 protein level.

Conclusions: Hyperioxia decreased AQP5 protein and mRNA expression, SB203580 and SP600125 up-regulated AQP5 expression.These data show that molecular pathway for AQP5 down-regulation effect in HLI may invovles p38 and JNK MAP Kinases.