Abstract
ABSTRACT Purpose The development and recovery(REC) of myopia is associated with changing of choroidal thickness(CT) in model of guinea pigs. Aquaporin-1 (AQP-1) is related to the changes of CT during the recovery from myopia, but the corresponding signaling pathway has not been clarified. This study aimed to investigate the effect of JNK1 on CT/AQP-1 and the recovery from myopia. Materials and Methods According to the different single intravitreal injections in eyes that underwent form deprivation for 21 days, guinea pigs were divided into four groups: the REC group, the REC+anisomycin (REC-AN, agonist for JNK1, 0.2 nmol) group, the REC+SP600125 (REC-SP, inhibitor for JNK1, 0.2 nmol) group, and the REC+dimethyl sulfoxide (REC-DM) group. Each group was divided into three subgroups based on the duration of the form deprivation: 3 days (d), 7 d and 10 d. All animals underwent biometric measurements (refractive error, axial length (AL), and CT), and the protein expression of AQP-1 and p-JNK1 in the choroid was also measured. Results In REC and REC-DM groups, significant differences in CT/refractive error/AL/p-JNK1 or AQP-1 were only found in the 3d group compared with normal control (NC) group (all p < .05). In REC-AN group, CT/p-JNK1 or AQP-1 in 3d group was significantly higher than that in other 3d groups (all p < .05), but no significant difference in refractive error or AL was found compared with NC group at three time points (all p > .05). In REC-SP group, a significant difference in refractive error/CT/p-JNK1 or AQP1 was found in 3d/7d group compared with NC group (all p < .05), but AL was only found in 3d groups (p = .001). Conclusions Changes in JNK1 phosphorylation can regulate AQP-1 and CT during the recovery from myopia and the recovery time. Thus, JNK1 may be a potential therapeutic target for preventing/treating myopia.
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