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H. Ren, G. Xu; Müller Cell Upregulate the Expression of SAP97 in Light-Injured Rat Retina. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2253.
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© ARVO (1962-2015); The Authors (2016-present)
To determined whether scaffolding protein family member synapse-associated protein 97 (SAP97) is involved in the Müller cell response to blue light injury.
Sprague-Dawley rats were exposed to intense blue light for 24 h. Transmission electron microscopy(TEM) was performed to evaluate the outer retina edema in light-injured retina.Cryosections and single isolated Müller cells were immunostained with SAP97, aquaporin-4(AQP4)and inwardly rectifying potassium channel Kir4.1 antibodies to detect the immunolocalization changes by confocal microscopy.Western blot and quantitative real-time PCR(qRT-PCR) were applied to evaluate the retinal SAP97,AQP4 and Kir4.1 protein and mRNA levels respectively.
In light-injured rats, obvious intracellular edema in the outer retina was observed by TEM. SAP97 was upregulated and concentrated in the outer nuclear layer after photic injury (Fig.1). The immunostaining of the AQP4 and Kir4.1 proteins were increased in the outer retina after light treatment which was similar with those changes of SAP97. Compared with control rat retina, retinal SAP97 mRNA in the light-exposed group was upregulated and maintained at a relatively high level. Whereas the mRNA levels of both Kir4.1 and AQP4 were increased at d1(the first after light exposure) and then declined at d2 and d3.Western blot showed that SAP97 and AQP4 protein levels were increased in d3 compared to control group(P<0.05),whereas the alteration of Kir4.1 protein level had no statistical significance.
Upregulation of SAP97 coincide with the redistribution of AQP4 and Kir4.1,suggesting that SAP97 play a major role in recruitment of such channels in light-induced outer retina edema.
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