ArticleBiochemical and biophysical research communications2020
Semaphorin 3A potentiates the profibrotic effects of transforming growth factor-β1 in the cornea.
Article in Biochemical and biophysical research communications, 2020. 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, 16 citations in OpenAlex.
- Single-cell transcriptomics reveals that tenocyte-derived MIF contributes to tendon injury pathogenesis.iScience · 2026Article
- Single-cell transcriptomic profiling identifies YY1 as a key regulator of fibroblast plasticity in hypertrophic scar formation.Burns & trauma · 2026Article
- Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts.Science immunology · 2025Article
- Regenerative Therapy for Corneal Scarring Disorders.Biomedicines · 2024Review
- Blocking Mitochondrial Pyruvate Transport Alters Corneal Myofibroblast Phenotype: A New Target for Treating Fibrosis.Investigative ophthalmology & visual science · 2023Article
- Review
- Regulation of Semaphorin3A in the process of cutaneous wound healing.Cell death and differentiation · 2022Review
- Defining the Role of Mitochondrial Fission in Corneal Myofibroblast Differentiation.Investigative ophthalmology & visual science · 2022Article
- The single nucleotide polymorphism rs1814521 in long non-coding RNA ADGRG3 associates with the susceptibility to silicosis: a multi-stage study.Environmental health and preventive medicine · 2022Article
- Semaphorin 3A-Glycosaminoglycans Interaction as Therapeutic Target for Axonal Regeneration.Pharmaceuticals (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Corneal scarring is a major cause of blindness worldwide with few effective therapeutic options. Finding a treatment would be of tremendous public health benefit, but requires a thorough understanding of the complex interactions that underlie this phenomenon. Here, we tested the hypothesis that the large increase in expression of Semaphorin 3A (SEMA3A) in corneal wounds contributes to the development of stromal fibrosis. We first verified this increased expression in vivo, in a cat model of photorefractive keratectomy-induced corneal wounding. We then examined the impact of adding exogenous SEMA3A to cultured corneal fibroblasts, and assessed how this affected the ability of transforming growth factor-beta1 (TGF-β1) to induce their differentiation into myofibroblasts. Finally, we examined how siRNA knockdown of endogenous SEMA3A affected these same phenomena. We found exogenous SEMA3A to significantly potentiate TGF-β1's profibrotic effects, with only a minimal contribution from cell-intrinsic SEMA3A. Our results suggest a previously unrecognized interaction between SEMA3A and TGF-β1 in the wounded cornea, and a possible contribution of SEMA3A to the regulation of tissue fibrosis and remodeling in this transparent organ.
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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.