Expression of Aquaporins in the Retina of Diabetic Rats

Abstract

Purpose/Aim: The development of retinal edema is the main reason of impaired vision in non-proliferative diabetic retinopathy. Water transport through aquaporins (AQPs) has been suggested to facilitate the development of ischemic edema in the retina. Here, we investigated whether experimental diabetic retinopathy in rats results in alterations of the AQP expression in the neural retina and retinal pigment epithelium (RPE).

Materials and Methods: Experimental diabetes in rats was induced by a single intravenous injection of streptozotocin (65 mg/kg body weight). The gene expression of AQPs in tissues from control and diabetic rats was examined by real-time RT-PCR. Retinal cryosections were immunostained against AQP5, 6, and 9.

Results: The total RNAs extracted from the neural retina and RPE contained gene transcripts for AQP0, 1, 3, 4, 5, 6, 8, 9, 11, and 12. Experimental diabetes was associated with an upregulation of AQP1 in the neural retina, and of AQP5, 9, 11, and 12 in the RPE. Furthermore, diabetes was associated with a downregulation of AQP6 and AQP11 in the neural retina, and of AQP0 in the RPE. AQP5 and AQP9 immunolabelings of the RPE were increased, and AQP6 labeling of the outer plexiform layer was decreased in retinal slices from diabetic rats in comparison to slices from control rats.

Conclusions: The data suggest that experimental diabetic retinopathy is associated with a complex pattern of alteration in the retinal AQP expression. These alterations might be involved in the adaptation of retinal cells to hyperglycemic conditions and the development and/or resolution of retinal edema.

Keywords::

• Aquaporin
• RT-PCR
• Immunohistochemistry
• Diabetic retinopathy
• Rat

ACKNOWLEDGMENTS

The authors thank Ute Weinbrecht and Franziska Rickers for excellent technical support. This work was supported by a grant from the Deutsche Forschungsgemeinschaft (KO 1547/6-1).

Declaration of interest: The authors report no conflict of interest. The authors alone are responsible for the content and writing of the paper.