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Ju, Meihua

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Ju, Meihua

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    SOCS3 in retinal neurons and glial cells suppresses VEGF signaling to prevent pathological neovascular growth
    (American Association for the Advancement of Science (AAAS), 2015) Sun, Ye; Ju, Meihua; Lin, Zhiqiang; Fredrick, T. W.; Evans, L. P.; Tian, Katherine; Saba, N. J.; Morss, P. C.; Pu, William; Chen, Jing; Stahl, A.; Joyal, Jean; Smith, Lois
    Accumulating evidence indicates that retinal neuroglia and neural cells contribute to neovascularization in proliferative retinopathy, but the controlling molecular interactions are not well known. We identified a mechanism by which neurons influence neovascularization through suppressor of cytokine signaling 3 (SOCS3) in neurons and glial cells. We found that Socs3 expression was increased in the retinal ganglion cell layer and inner nuclear layer after oxygen- induced retinopathy. Neuronal/glial Socs3 deficient mice with oxygen-induced retinopathy had significantly increased pathologic retinal neovascularization and reduced vaso-obliterated retinal areas, suggesting that loss of neuronal/glial SOCS3 increased both retinal vascular re-growth and pathological neovascularization. In response to oxygen-induced retinopathy, retinal vascular endothelial growth factor A (Vegfa) expression was higher in neuronal/glial Socs3 deficient mice than in than Socs3 flox/flox controls indicating that neuronal and glial Socs3 suppressed Vegfa during pathologic conditions. Lack of neuronal/glial SOCS3 resulted in greater phosphorylation and activation of STAT3, which led to increased expression of its gene target Vegfa, and increased endothelial cell proliferation. In summary, neuronal/glial SOCS3 suppresses endothelial cell activation through suppression of STAT3-mediated neuronal/glia VEGF secretion, resulting in less endothelial proliferation and angiogenesis. These results show that neuronal/glial SOCS3 regulates neurovascular interaction and pathologic retinal angiogenesis by titrating VEGF signaling.