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- W2999364593 abstract "Diabetic retinopathy (DR) is a common complication of diabetes and leads to blindness. Anti-VEGF is a primary treatment for DR. Its therapeutic effect is limited in non- or poor responders despite frequent injections. By performing a comprehensive analysis of the semaphorins family, we identified the increased expression of Sema4D during oxygen-induced retinopathy (OIR) and streptozotocin (STZ)-induced retinopathy. The levels of soluble Sema4D (sSema4D) were significantly increased in the aqueous fluid of DR patients and correlated negatively with the success of anti-VEGF therapy during clinical follow-up. We found that Sema4D/PlexinB1 induced endothelial cell dysfunction via mDIA1, which was mediated through Src-dependent VE-cadherin dysfunction. Furthermore, genetic disruption of Sema4D/PlexinB1 or intravitreal injection of anti-Sema4D antibody reduced pericyte loss and vascular leakage in STZ model as well as alleviated neovascularization in OIR model. Moreover, anti-Sema4D had a therapeutic advantage over anti-VEGF on pericyte dysfunction. Anti-Sema4D and anti-VEGF also conferred a synergistic therapeutic effect in two DR models. Thus, this study indicates an alternative therapeutic strategy with anti-Sema4D to complement or improve the current treatment of DR." @default.
- W2999364593 created "2020-01-23" @default.
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- W2999364593 date "2020-01-13" @default.
- W2999364593 modified "2023-10-15" @default.
- W2999364593 title "Inhibition of Sema4D/PlexinB1 signaling alleviates vascular dysfunction in diabetic retinopathy" @default.
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- W2999364593 doi "https://doi.org/10.15252/emmm.201810154" @default.
- W2999364593 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7005627" @default.
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- W2999364593 hasPublicationYear "2020" @default.
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