ArticleScientific reports2024
Transcription factor 4 promotes increased corneal endothelial cellular migration by altering microtubules in Fuchs endothelial corneal dystrophy.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Biomaterial-Assisted Strategies in Corneal Endothelial Cell Therapy: Toward a Platform-Based Approach.Pharmaceutics · 2026Review
- Pathological classification of Fuchs endothelial corneal dystrophy into several types and their relationships with CTG18.1 expansion repeats.The Journal of pathology · 2026Article
- A molecular and spatial resource defining tubulin isotype organization during corneal development.bioRxiv : the preprint server for biology · 2026Article
- Transcription factor 4 and Fuchs' endothelial corneal dystrophy (FECD) association: Perspectives for novel targeted therapeutics.Eye (London, England) · 2025Article
- Transcriptome analyses of human corneal endothelial cell lines derived from patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Bioengineering Strategies for Corneal Endothelial Cell Injection Therapy: Advances, Challenges, and Clinical Translation.Bioengineering (Basel, Switzerland) · 2025Review
- TGF-β Promotes Endothelial-to-Mesenchymal Transition and Alters Corneal Endothelial Cell Migration in Fuchs Endothelial Corneal Dystrophy.International journal of molecular sciences · 2025Article
- Review
- Article
- Assessment of Early Fuchs Endothelial Corneal Dystrophy and CTG Trinucleotide Expansion Positivity Using Scheimpflug Imaging.Ophthalmology scienceArticle
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fuchs endothelial corneal dystrophy (FECD) is a complex corneal disease characterized by the progressive decline and morphological changes of corneal endothelial cells (CECs) that leads to corneal edema and vision loss. The most common mutation in FECD is an intronic CTG repeat expansion in transcription factor 4 (TCF4) that leads to its altered expression. Corneal endothelial wound healing occurs primarily through cell enlargement and migration, and FECD CECs have been shown to display increased migration speeds. In this study, we aim to determine whether TCF4 can promote cellular migration in FECD CECs. We generated stable CEC lines derived from FECD patients that overexpressed different TCF4 isoforms and investigated epithelial-to-mesenchymal (EMT) expression, morphological analysis and cellular migration speeds. We found that full length TCF4-B isoform overexpression promotes cellular migration in FECD CECs in an EMT-independent manner. RNA-sequencing identified several pathways including the negative regulation of microtubules, with TUBB4A (tubulin beta 4A class IVa) as the top upregulated gene. TUBB4A expression was increased in FECD ex vivo specimens, and there was altered expression of cytoskeleton proteins, tubulin and actin, compared to normal healthy donor ex vivo specimens. Additionally, there was increased acetylation and detyrosination of microtubules in FECD supporting that microtubule stability is altered in FECD and could promote cellular migration. Future studies could be aimed at investigating if targeting the cytoskeleton and microtubules would have therapeutic potential for FECD by promoting cellular migration and regeneration.
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