Upregulation of SOX9 in Glial (Müller) cells in retinal light damage of rats.

Recent evidence suggests that SOX9 [sex-determining region Y (SRY) box 9], a transcription factor, plays a pivotal role in acquired diseases, revealing its importance in roles beyond development. However, whether SOX9, which is one of the key regulators of retinal Müller cell development, also participates in the pathological process of retinal degenerative diseases remains unknown. In the present study, we hypothesized that SOX9 was upregulated in Müller cells in retinal degeneration. Retinal light damage (LD) was used as a model for retinal degeneration. On day 3, 7, 14, 21, and 28 after LD in adult Sprague Dawley (SD) rats, the spatial distribution of SOX9 in the retina was observed by immunohistochemistry; the expression levels of SOX9 were measured by real-time PCR and Western blot analysis. Moreover, type 1 collagen (COL1) and cone-rod homeobox (CRX) protein levels, which are two downstream targets of SOX9, were also assessed by Western blot analysis. Colabeling for SOX9 and glutamine synthetase (GS), a specific Müller cell maker, indicated that SOX9 was expressed in the Müller cell nucleus in both control and LD groups. Significantly enhanced SOX9 expression was observed as early as day 3 after LD, and it persisted for at least 28 days. COL1 and CRX protein levels also increased after LD. Our study demonstrates the involvement of SOX9 in acquired retinal degeneration triggered by LD, which might provide novel insights into possible molecular mechanisms that would account for the involvement of Müller cells in retinal degenerative diseases.