Expression of Aquaporins in the Inner Ear of Normal Guinea Pigs and Guinea Pigs with Endolymphatic Hydrops / 听力学及言语疾病杂志

ABSTRACT

Objective To study the expression of aquaporins(AQPs) in the inner ear of normal guinea pig and guinea pigs with endolymphatic hydrops, and to investigate the mechanism and significance. Methods The guinea pigs were divided into two groups randomly model group and control group. The guinea pigs in model group were given desmopressing 4 ?g?kg-1?d-1 introperitoneally for 1 week, while the guinea pigs in control group were given saline. After one week, the expression of AQPs in the inner ears of all guinea pigs was evaluated.Results Expression of AQP0, 1, 2, 3, 5, 7 and 8 were found in the ears of normal guinea pigs. Weak expression of AQP0 was found in stria vascularis and spiral ganglion. The distribution of AQP1 consisted of cellular lining the bony labyrinth, fibrocytes lining in the endolymphatic duct and sac, cells under the basilar membrane, fibrocytes of the spiral ligament and the spiral limbus, Corti's organ, inner and outer spiral sulcus, stria vascularis, saccular and utricular wall, and spiral ganglion. AQP2 were found in stria vascularis, Corti's organ, spiral ganglion and endolymphatic sac. AQP3, 7 and 8 were distributed in a similar manner as the surrounding membranous labyrinth, including Corti's organ, inner and outer spiral sulcus, stria vascularis, fibrocytes of the spiral ligament and the spiral limbus, saccular and utricular wall, endolymphatic sac and spiral ganglion. AQP5 was found at Corti's organ, inner and outer spiral sulcus, spiral ganglion and fibrocytes in spiral ligment. The AQP2 in stria vascularis and endolymphatic sac was stronger in the inner ears with ELH than that in normal ears.Conclusion There are various AQPs in inner ears of normal guinea pigs, and their distributions are overlapping and without obvious regional specificity. Desmopressing induces the expression of AQP2 in the inner ears of guinea pigs. The results indicate that ELH may correlate to upregulation of AQP2, but the mechanism remains unclear.