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Y. Luo, W. Xiao, J. Li, X. Zhu, T. Li, X. Liu, S. Tang; mRNA Expression Patterns of Claudins in the Normal and Oxygen-Induced Retinopathy Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3132.
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© ARVO (1962-2015); The Authors (2016-present)
Claudins (Cldns), comprising 24 members, are key regulators for tight junction of epithelial and endothelial cells. Accumulating data indicate that the expression of claudins change in many physiological and pathophysiological conditions. The present study was to elucidate the mRNA expression patterns of claudins in the retina of normal and oxygen-induced retinopathy (OIR) mice.
In our study, postnatal 7(P7) C57BL/6 mice were exposed to a chamber with a 75% concentration of oxygen, and then returned to room air when they were P12 to induce retinal neovascularization. FITC-dextran perfusion was used to assess retinal neovasculature. Function of inner blood-retinal barrier was quantitatively evaluated by Evans blue perfusion. At P8, 11, 13, 15, 18 and 21, quantitative real-time RT-PCR was used to measure the mRNA level of claudin subtypes in the retina of normal and OIR mice.
Plenty of retinal neovasculatures were observed in OIR mice. Dramatic leakage of Evans blue was detected in OIR mice retina. Real-time RT-PCR showed that during the normal development of mouse retina, cldn-12 was the most abundant subtype, followed by cldn-5, -7 and -23; The expression of cldn-7, -10, -11, -12 and ZO-1 were stable. The mRNA level of cldn-1, -2, -8, -9, -13, -16, -19, -22 and -23 displayed an increasing manner, whereas the mRNA level of cldn-14 was decreasing along with time. In OIR mice, the mRNA level of cldn 1-5, 7-17, -19, -22, -23 were not changed too much under hyperxia condition(P7-P12) , then upregulated under the following relative hypoxia condition (P13-P18), especially cldn-5, -19 and -23. At P21, cldn-4 and cldn-5 was downregulated to a level lower than those of P8. Cldn-6 was detected in the retina of neither normal nor OIR mice.
This study indicates that inner blood-retinal barrier is seriously damaged in OIR mice. Cldn-5 and -23 may be responsible for the formation and mature of tight junction during the normal retinal development and the inner blood-retinal barrier dysfunction induced by hypoxia.
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