ArticleGraefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie2016
S100A4 gene silencing in oxygen-induced ischemic retinopathy inhibits retinal neovascularization via down-regulation of CREB expression.
Article in Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Inhibition of TLR4/NF-κB pathway and endoplasmic reticulum stress by overexpressed S100A4 ameliorates retinal ischemia-reperfusion injury of mice.Molecular neurobiology · 2024Article
- Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022Review
- S100A4 Silencing Facilitates Corneal Wound Healing After Alkali Burns by Promoting Autophagy via Blocking the PI3K/Akt/mTOR Signaling Pathway.Investigative ophthalmology & visual science · 2020Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the possible role of S100A4 in retinal neovascularization (RNV), as well as the underlying mechanism, in a mouse model of oxygen-induced retinopathy (OIR).
methodsRetinas used in the experiments were obtained from a mouse model of OIR with and without treatment by intravitreal injection of adnoviral-S100A4-RNAi or adenoviral-green fluorescent protein at postnatal day 12 (P12). At P17, the efficacy of adenoviral gene transfer was assessed with fluorescence microscopy. RNV was evaluated by whole-mount immunofluorescent staining of the mouse retina with Griffonia simplicifolia isolectin B4 conjugated to Alexa Fluor 594 and quantified by counting the number of pre-retinal neovascular cells. Protein and mRNA expression levels of S100A4, cyclic AMP (cAMP) response element-binding protein (CREB), B-cell lymphoma 2 (Bcl-2), and caspase-3 were determined using Western blot analysis and real-time PCR.
resultsRetinal S100A4 levels were positively correlated with the progression of RNV. In the intravitreal Ad-S100A4-RNAi transfer mice, both S100A4 protein and mRNA expression levels in the retina were significantly decreased at P17. Ad-S100A4-RNAi transfer was clearly demonstrated by the green fluorescent protein (GFP) in many layers of the retina, including the ganglion cell layer (GCL), inner plexiform layer (IPL), inner nuclear layer (INL), outer plexiform layer (OPL), and outer nuclear layer (ONL), 3 days after intravitreal injection. Whole-mount immunofluorescent staining of the retina and quantification of the pre-retinal neovascular cells demonstrated that RNV was significantly ameliorated. At the same time, the expression of CREB and Bcl-2 were significantly decreased at the transcriptional and translational levels in the OIR-S100A4 group, whereas caspase-3 expression was increased.
conclusionsOur results indicated that RNV was ameliorated by Ad-S100A4-RNAi transfer in a mouse model of OIR through mediation of the anti-apoptotic effect of Bcl-2 by reducing the expression of CREB, and that S100A4 may be a novel therapeutic target for ocular neovascularization diseases.
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