ArticleInvestigative ophthalmology & visual science2024
Lack of Elevated Expression of TGFβ3 Contributes to the Delay of Epithelial Wound Healing in Diabetic Corneas.
Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Fatty Acid Desaturase 1 Knockdown Promotes Wound Healing and Functional Recovery of the Corneal Epithelium in Diabetes.Investigative ophthalmology & visual science · 2025Article
- Conditioned media of stem cells from human exfoliated deciduous teeth contain factors related to extracellular matrix organization and promotes corneal epithelial wound healing.Regenerative therapy · 2025Article
- Prox1 Protein in Corneal Limbal Lymphatic Vessels Maintains Limbal Stem Cell Stemness and Regulates Corneal Injury Repair.Investigative ophthalmology & visual science · 2025Article
- Norepinephrine regulates epithelial-derived neurotrophins expression and sensory nerve regeneration through ADRB2 receptor.Communications biology · 2025Article
- Evaluating Therapeutic and Chemical Toxicity Using Organ-Cultured Porcine Corneas and Epithelial Wound Healing.Journal of visualized experiments : JoVE · 2025Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Purpose: To investigate the mechanisms underlying the differential roles of TGFβ1 and TGFβ3 in accelerating corneal epithelial wound healing (CEWH) in diabetic (DM) corneas, with normoglycemia (NL) corneas as the control. Methods: Two types of diabetic mice, human corneal organ cultures, mouse corneal epithelial progenitor cell lines, and bone marrow-derived macrophages (BMDMs) were employed to assess the effects of TGFβ1 and TGFβ3 on CEWH, utilizing quantitative PCR, western blotting, ELISA, and whole-mount confocal microscopy. Results: Epithelial debridement led to an increased expression of TGFβ1 and TGFβ3 in cultured human NL corneas, but only TGFβ1 in DM corneas. TGFβ1 and TGFβ3 inhibition was significantly impeded, but exogenous TGFβ1 and, more potently, TGFβ3 promoted CEWH in cultured TKE2 cells and in NL and DM C57BL6 mouse corneas. Wounding induced similar levels of p-SMAD2/SMAD3 in NL and DM corneas but weaker ERK1/2, Akt, and EGFR phosphorylation in DM corneas compared to NL corneas. Whereas TGFβ1 augmented SMAD2/SMAD3 phosphorylation, TGFβ3 preferentially activated ERK, PI3K, and EGFR in healing DM corneas. Furthermore, TGFβ1 and TGFβ3 differentially regulated the expression of S100a9, PAI-1, uPA/tPA, and CCL3 in healing NL and DM corneas. Finally, TGFβ1 induced the expression of M1 macrophage markers iNOS, CD86, and CTGF, whereas TGFβ3 promoted the expression of M2 markers CD206 and NGF in BMDMs from db/db or db/+ mice. Conclusions: Hyperglycemia disrupts the balanced expression of TGFβ3/TGFβ1, resulting in delayed CEWH, including impaired sensory nerve regeneration in the cornea. Supplementing TGFβ3 in DM wounds may hold therapeutic potential for accelerating delayed wound healing in diabetic patients.
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Registered trials
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