ArticleVascular cell2016
A novel endothelial-derived anti-inflammatory activity significantly inhibits spontaneous choroidal neovascularisation in a mouse model.
Article in Vascular cell, 2016. 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.
- JR5558 mice are a reliable model to investigate subretinal fibrosis.Scientific reports · 2024Article
- Review
- Identification of Novel Choroidal Neovascularization-Related Genes Using Laplacian Heat Diffusion Algorithm.BioMed research international · 2021Article
- Chronic Dicer1 deficiency promotes atrophic and neovascular outer retinal pathologies in mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Targeting the Notch and TGF-β signaling pathways to prevent retinal fibrosisTheranostics · 2020Article
- Spontaneous Posterior Segment Vascular Disease Phenotype of a Mouse Model, rnv3, Is Dependent on the Crb1rd8 Allele.Investigative ophthalmology & visual science · 2018Article
- Retinal Vasculature in Development and Diseases.Annual review of vision science · 2018Review
- Inhibition of YAP ameliorates choroidal neovascularization via inhibiting endothelial cell proliferation.Molecular vision · 2018Article
- The effect of anagliptin on intimal hyperplasia of rat carotid artery after balloon injury.Molecular medicine reports · 2017Article
- Animal models of ocular angiogenesis: from development to pathologies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Review
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Authors and funding
2 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundEndothelial cells (EC) grown on collagen particles inhibit intimal hyperplasia in animal models when applied perivascularly, and this effect appears to be, at least in part, the result of EC-derived soluble factors that suppress local vascular inflammation. To elucidate the molecular basis of the therapeutic effects of EC grown on collagen particles, the anti-inflammatory activity of conditioned medium from these cells was characterized.
methodsHuman aortic EC (HAEC) and, for chromatin immunoprecipitation assays, human umbilical vein EC (HUVEC) were treated with tumor necrosis factor alpha (TNFα) in the presence of conditioned medium generated by HAEC grown on collagen particles (ECPCM), and the anti-inflammatory effects were evaluated by analysing the expression of the inflammation-related adhesion molecules E-selectin and vascular cell adhesion molecule-1 (VCAM-1). The therapeutic activity of ECPCM was studied using the mouse strain JR5558, which develops spontaneous choroidal neovascularisation (CNV) lesions driven by local inflammation.
resultsECPCM significantly suppressed TNFα-induced expression of E-selectin and VCAM-1. ECPCM did not affect the mRNA stability of the two genes, but suppressed TNFα-induced binding of the p65 subunit of NF-kB transcription factor to E-selectin and VCAM-1 promoters. In vivo, systemic ECPCM treatment significantly reduced the CNV area and the recruitment of activated macrophages to the lesions. Characterization of the molecule responsible for the anti-inflammatory activity in ECPCM indicates that it is unlikely to be a protein and that it is not any of the better characterized EC-derived anti-inflammatory molecules.
conclusionsMedium conditioned by HAEC grown on collagen particles exhibits significant anti-inflammatory activity via inhibition of genes that mediate inflammatory responses in EC.
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