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Research Letter |

Alteration of Vitreal Retinoschisin Level in Human Primary Retinal Detachment

Sten Kjellström, MD, PhD1; Fredrik Ghosh, MD, PhD1; Camasamudram Vijayasarathy, PhD2; Sten Andréasson, MD, PhD1
[+] Author Affiliations
1Department of Ophthalmology, University of Lund, Lund, Sweden
2National Institute of Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland
JAMA Ophthalmol. 2014;132(3):353-354. doi:10.1001/jamaophthalmol.2013.6306.
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Retinoschisin (RS1), the product of RS1 located on the X chromosome, is expressed mainly in retina.1 The 24-kDa RS1 encodes a highly conserved sequence motif termed the discoidin domain, which is a critical determinant of the structural and functional integrity of the retina.2 Mutations in RS1 that lead to either complete loss of RS1 expression or its accumulation as a nonfunctional misfolded form are the underlying causes of X-linked retinoschisis (XLRS).3 This disorder, seen exclusively in young males, is characterized by splitting, or schisis, affecting all retinal layers. The precise molecular mechanism by which RS1 functions is still undefined. During development, there is a wave of RS1 expression beginning at the retinal surface and spreading progressively in more distal retinal layers as they differentiate.4 In adult mice, RS1 is expressed in all retinal neurons except horizontal cells,4 with a predominance in photoreceptor inner segments and bipolar cells.

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Quantitation of Retinoschisin in Vitreous From Newly Detached and Nondetached Retinas

The nondetached retina uses the epiretinal membrane for analysis. RS1 indicates retinoschisin; center horizontal lines, mean; and error bars, standard error.

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