Aquaporin‐4 and potassium channel kir4.1 in amd and serous retinal detachment secondary to choroidal melanoma

Abstract

Purpose Aquaporin‐4 (AQP4) and potassium channel Kir4.1 are normally expressed in retinal Müller glia, and play a major role in controlling retinal fluid and maintaining retinal integrity and function. We examined AQP4 and Kir4.1 distribution and expression in human eyes with late age‐related macular degeneration (AMD) or long‐term serous retinal detachment secondary to choroidal melanoma. Methods Paraffin sections of central and peripheral choroid/retina from young (<40 years, n=5), aged (>70 years, n=4) and AMD (>70 years, n=5) human post‐mortem eyes, and whole human eyes with choroidal melanoma (n=5), were co‐immunolabelled with antibodies to AQP4, Kir4.1 and GFAP, and visualised using immunofluoresence and confocal microscopy. Results We found differential expression of AQP4 and Kir4.1 in detached retina of melanoma eyes, with upregulation of AQP4 and downregulation of Kir4.1 compared to unaffected eyes. This was most obvious in the retina overlying melanomas and in detached retina separated from underlying choroid. GFAP immunoreactitvity was upregulated in areas of serous retinal detachment, and retinal thinning; Müller cell processes extended along the anterior surface of melanomas. No apparent difference in distribution or expression of AQP4 or Kir4.1 was observed for retinas with late stage AMD compared to controls. Conclusion Decreased Kir4.1 expression in long term serous retinal detachment may be associated with Müller cell proliferative gliosis, as suggested in earlier animal studies. Increased AQP4 expression suggests efforts to restore retinal fluid balance in areas with photoreceptor degeneration and compromised outer blood‐retinal barrier. Support: NFMRI (MCM), Lions NSW Eye Eyebank