Interleukin 37 promotes angiogenesis through TGF-β signaling

Abstract IL-37 is a novel pro-angiogenic cytokine that potently promotes endothelial cell activation and pathological angiogenesis in our previous study, but the mechanisms behind the pro-angiogenic effect of IL-37 are less well understood. Extending our observations, we found that TGF-β interacts w...

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Autores principales: Mengmeng Zhao, Yongguang Hu, Jiayi Jin, Ying Yu, Shanshan Zhang, Jingjing Cao, Yuanfen Zhai, Rongbin Wei, Juanjuan Shou, Wenping Cai, Shangfeng Liu, Xiaoping Yang, Guo-Tong Xu, Jianhua Yang, David B. Corry, Shao Bo Su, Xialin Liu, Tianshu Yang
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/e73b8ca65f3f4f5c849d6edbe4ff39d1
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Sumario:Abstract IL-37 is a novel pro-angiogenic cytokine that potently promotes endothelial cell activation and pathological angiogenesis in our previous study, but the mechanisms behind the pro-angiogenic effect of IL-37 are less well understood. Extending our observations, we found that TGF-β interacts with IL-37, and potently enhances the binding affinity of IL-37 to the ALK1 receptor complex, thus allowing IL-37 to signal through ALK1 to activate pro-angiogenic responses. We further show that TGF-β and ALK1 are required in IL-37 induced pro-angiogenic response in ECs and in the mouse model of Matrigel plug and oxygen-induced retinopathy. The result suggests that IL-37 induces pro-angiogenic responses through TGF-β, which may act as the bridging molecule that mediates IL-37 binding to the TGF-β receptor complex.