ArticleScientific reports2017
Generation of a new mouse model of glaucoma characterized by reduced expression of the AP-2β and AP-2δ proteins.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Deletion of ARPKD-associated Pkhd1 gene in mice results in decreased Tfap2b expression and eye abnormalities.Nature communications · 2026Article
- Studies of mice with a large deletion of the ARPKD-associatedbioRxiv : the preprint server for biology · 2026Article
- High-resolution genome topology of human retina uncovers super enhancer-promoter interactions at tissue-specific and multifactorial disease loci.Nature communications · 2022Article
- Deletion of transcription factor AP-2β from the developing murine trabecular meshwork region leads to progressive glaucomatous changes.Journal of neuroscience research · 2022Article
- Conditional Deletion of AP-2β in the Periocular Mesenchyme of Mice Alters Corneal Epithelial Cell Fate and Stratification.International journal of molecular sciences · 2021Article
- A Minimally Invasive Experimental Model of Acute Ocular Hypertension with Acute Angle Closure Characteristics.Translational vision science & technology · 2020Article
- AP-2β is required for formation of the murine trabecular meshwork and Schlemm's canal.Experimental eye research · 2020Article
- Relationship between neural crest cell specification and rare ocular diseases.Journal of neuroscience research · 2019Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We generated 6 transgenic lines with insertion of an expression plasmid for the R883/M xanthine dehydrogenase (XDH) mutant protein. Approximately 20% of the animals deriving from one of the transgenic lines show ocular abnormalities and an increase in intra-ocular pressure which are consistent with glaucoma. The observed pathologic phenotype is not due to expression of the transgene, but rather the consequence of the transgene insertion site, which has been defined by genome sequencing. The insertion site maps to chromosome 1qA3 in close proximity to the loci encoding AP-2β and AP-2δ, two proteins expressed in the eye. The insertion leads to a reduction in AP-2β and AP-2δ levels. Down-regulation of AP-2β expression is likely to be responsible for the pathologic phenotype, as conditional deletion of the Tfap2b gene in the neural crest has recently been shown to cause defective development of the eye anterior segment and early-onset glaucoma. In these conditional knock-out and our transgenic mice, the morphological/histological features of the glaucomatous pathology are surprisingly similar. Our transgenic mouse represents a model of angle-closure glaucoma and a useful tool for the study of the pathogenesis and the development of innovative therapeutic strategies.
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