ArticleJournal of cell science2011
Notch gain of function in mouse periocular mesenchyme downregulates FoxL2 and impairs eyelid levator muscle formation, leading to congenital blepharophimosis.
Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Variant Curation of the Largest Compendium ofHuman mutation · 2026Article
- Excess Transforming Growth Factor-α Changed the Cell Properties of Corneal Epithelium and Stroma.Investigative ophthalmology & visual science · 2020Article
- Aberrant expression of a stabilized β-catenin mutant in keratocytes inhibits mouse corneal epithelial stratification.Scientific reports · 2019Article
- Generation and Characterization of a Novel Mouse Line, Keratocan-rtTA (KeraRT), for Corneal Stroma and Tendon Research.Investigative ophthalmology & visual science · 2017Article
- Perturbed meibomian gland and tarsal plate morphogenesis by excess TGFα in eyelid stroma.Developmental biology · 2015Article
- Wnt/β-catenin signaling modulates corneal epithelium stratification via inhibition of Bmp4 during mouse development.Development (Cambridge, England) · 2015Article
- FOXL2 modulates cartilage, skeletal development and IGF1-dependent growth in mice.BMC developmental biology · 2015Article
- Eyelid closure in embryogenesis is required for ocular adnexa development.Investigative ophthalmology & visual science · 2014Article
- Article
- Lumican binds ALK5 to promote epithelium wound healing.PloS one · 2013Article
- Wakayama Symposium: Notch-FoxL2-α-SMA axis in eyelid levator muscle development and congenital blepharophimosis.The ocular surface · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Notch signaling is pivotal for the morphogenesis and homeostasis of many tissues. We found that aberrant Notch activation in mouse neural-crest-derived periocular mesenchymal cells (POMCs), which contribute to the formation of corneal and eyelid stroma, results in blepharophimosis. Compound transgenic mice overexpressing the Notch1 intracellular domain (N1-ICD) in POMCs (POMC(N1-ICD)) showed relatively minor effects on the cornea, but increased cell apoptosis and decreased cell proliferation during eyelid morphogenesis. Eyelid closure at E15.5 and eyelid formation at birth were incomplete. In further analyses, overexpression of N1-ICD impaired eyelid levator smooth muscle formation by downregulating the transcription factor FoxL2. This is similar to the effect of haploinsufficiency of FOXL2 in humans, which results in type II BPES (blepharophimosis, ptosis and epicanthus inversus syndrome). In vitro studies showed that FoxL2 expression is augmented by a low dose of N1-ICD but was downregulated by a high dose, depending on the extent of Hes-1 and Hey-1 activation. Moreover, transfection of CMV-FoxL2 enhanced α-SMA promoter activity. These data strongly imply that a physiologically low level of Notch1 is crucial for proper FoxL2 expression in POMCs, which is, in turn, essential for Müeller muscle formation and normal eyelid development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.