ArticleScientific reports2020
A fine-tuned β-catenin regulation during proliferation of corneal endothelial cells revealed using proteomics analysis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- A Cross-Species Hydroquinone Model Replicates Smoking-Related Corneal Endothelial Oxidative Injury and Enables Therapeutic Screening of FGF10.Investigative ophthalmology & visual science · 2026Article
- Bioengineering Strategies for Corneal Endothelial Cell Injection Therapy: Advances, Challenges, and Clinical Translation.Bioengineering (Basel, Switzerland) · 2025Review
- Excess Wnt in neurological disease.The Biochemical journal · 2025Review
- Specular microscopy of the corneal endothelial cells of bovines: anOpen veterinary journal · 2023Article
- Decoding the Human Epidermal Complexity at Single-Cell Resolution.International journal of molecular sciences · 2023Review
- Nanoneedles Induce Targeted siRNA Silencing of p16 in the Human Corneal Endothelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Fluctuations in Corneal Endothelial LAP2 Expression Levels Correlate with Passage Dependent Declines in Their Cell Proliferative Activity.International journal of molecular sciences · 2022Article
- Altered gene expression in slc4a11Scientific reports · 2021Article
- Regenerative Medicine of Epithelia: Lessons From the Past and Future Goals.Frontiers in bioengineering and biotechnology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Corneal endothelial (CE) dysfunction is the main indication for corneal transplantation, an invasive procedure with several limitations. Developing novel strategies to re-activate CE regenerative capacity is, therefore, of fundamental importance. This goal has proved to be challenging as corneal endothelial cells (CEnC) are blocked in the G0/G1 phase of the cell cycle in vivo and, albeit retaining proliferative capacity in vitro, this is further hindered by endothelial-to-mesenchymal transition. Herein we investigated the mechanisms regulating CEnC proliferation in vitro. Comparing the proteome of non-proliferating (in vivo-G0/G1) and proliferating (in vitro-G2/M) rabbit CEnC (rCEnC), 77 proteins, out of 3,328 identified, were differentially expressed in the two groups (p < 0.005). Literature and Gene Ontology analysis revealed β-catenin and transforming growth factor (TGF-β) pathways to be correlated with the identified proteins. Treatment of rCEnC with a β-catenin activator and inhibitor showed that β-catenin activation was necessary during rCEnC proliferation, but not sufficient for its induction. Furthermore, both pro-proliferative activity of basic fibroblast growth factor and anti-proliferative effects of TGF-β were regulated through β-catenin. Overall, these results provide novel insights into the molecular basis underlying the proliferation process that CEnC re-activate in vitro, consolidating the role of β-catenin and TGF-β.
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Registered trials
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