Morphologic and histopathologic change of sodium iodate-induced retinal degeneration in adult rats.

Adult teleost fish are capable of regenerating their retinas following injury. In contrast, the adult mammalian retina has little capacity for regeneration. Here, we describe the morphologic and histopathologic course of sodium iodate (NaIO) injection on rat retinas. A single dose of NaIO (50 mg/kg) was administered intravenously to adult Sprague-Dawley male rats. Control animals received sodium chloride. Morphologic and molecular changes following NaIO injection were monitored by histological and gene expression analysis. We observed retinal pigment epithelium (RPE) cell death began at 6 h PI. After 3 and 7 days, we found local tissue repair by RPE cell regeneration. This was further confirmed by a significant decrease in photoreceptor cell apoptosis in the outer nuclear layer. Protein-level analysis demonstrated the attenuated regulation of cellular markers specially related to active gliosis in retinal Müller cells, including cellular retinaldehyde-binding protein (CRALBP) and glutamine synthetase (GS), after NaIO treatment for 3rd and 7th days. The Müller cells exhibited signs of dedifferentiation, as paired box 6 (PAX6) and SRY box 2 (SOX2) were expressed by NaIO stimulated Müller glia proliferation and overexpression of proliferating cell nuclear antigen (PCNA). We concluded that NaIO injection can result in significant and progressive damage to RPE and photoreceptor cells. Our observations suggest that Müller cell transient differentiation and RPE recovery is induced in the mammalian retina by relatively high doses of NaIO. Transient change in Müller cell differentiation and RPE cell recovery may result in photoreceptor apoptosis decrease.