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N. Katai, A. Sato, N. Yoshida, N. Gotoh, T. Kikuchi, H. Shibuki, N. Yoshimura; Nonrefractive role of beta–crystallin in the retinal neovascularization . Invest. Ophthalmol. Vis. Sci. 2004;45(13):487.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Although beta–crystallins had been considered for a long time to be present only in the ocular lens and structural protein to maintain the transparency of the lens, recently extralenticular expression in normal and pathological state was indicated. However, nonrefractive function was totally unknown. Our purpose is to characterize the role of beta–crystallin expressing in the early stage of retinal neovascularization. Methods: Neonatal C57BL/6J mice with their nursing mother were exposed to 75% oxygen from P5 to P12 and then returned to room air to produce retinal neovascularization. Control mice were kept in room air. Eyes were enucleated at P13, P14, P15, and P17. Localization of beta–crystallin is determined by immunohistochemical methods. Synthetic siRNAs were delivered in vivo at P12, P14 and P16 after exposure to hyperoxia. The number of the glomerular tufts formed was quantified by counting the total number of glomerular tufts at P15. Neovascularization was quantified by counting the number of nuclei that were located on the vitreous side of the internal limiting membrane. Results: Beta–crystallin is expressed selectively in astrocytes of glomerular tufts in the model of retinal neovascularization. Reduction of beta–crystallin transcripts effectively inhibited glomerular tuft formation and development of retinal neovascularization. Conclusions: Extralenticular expressed beta–crystallin play an important role in the glomerular tuft formation and development of retinal neovascularization. Thus, drugs inhibiting beta–crystallin expression may have a value in the treatment of retinal neovascular diseases.
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