ArticleGenes2024
Kir4.1 and Aqp4 Contribution to Schisis Cystic Water Accumulation and Clearance in the Rs1 Exon-1 Del XLRS Rat Model.
Article in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Modulation of Systemic Osmolarity Alters Retinal Thickness and Schisis Cavities Without Blood Retinal Barrier Disruption in Rs1 Knockout Mice.Investigative ophthalmology & visual science · 2026Article
- Microglial phagocytosis of bipolar cells triggers inner retinal degeneration in Rs1-KO mice.Cell communication and signaling : CCS · 2026Article
- Article
- Angle closure glaucoma in a patient with X-linked retinoschisis: a case report.International journal of ophthalmology · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
BACKGROUND/
objectiveThe Rs1 exon-1-del rat (Rs1KO) XLRS model shows normal retinal development until postnatal day 12 (P12) when small cystic spaces start to form in the inner nuclear layer. These spaces enlarge rapidly, peak at P15, and then collapse by P19.
methodsWe explored the possible involvement of Kir4.1 and Aqp4, the principal retina channels for water movement and homeostasis, along with Muller glia cells (MGCs), using semi-quantitative fluorescent immunohistochemistry at P7, P9, P12, and P30, in Rs1KO and WT littermates.
resultsKir4.1 expression was reduced in Rs1KO retinas at all the early time points-P7, P9, and P12-as the schisis cavities began to form; downregulation would reduce water egress from the retina. Aqp4 was upregulated at P30 in Rs1KO retinas during schisis cavity closure but not as cavities formed at P12. When examined by GFAP expression, MGCs were not activated at the preschisis P12 age but showed considerable GFAP expression at P30 following retinal cystic structural damage at P15, indicating that MGCs were activated during the period of retina water removal and cavity closure.
conclusionsThe study results implicate the downregulation of Kir4.1 in schisis formation and a role for both Kir4.1 and Aqp4 upregulation in subsequent schisis closure.
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