Interleukin 37 promotes angiogenesis through TGF-β signaling

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

doi:10.1038/s41598-017-06124-z

Interleukin 37 promotes angiogenesis through TGF-β signaling

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

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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.

Original language	English (US)
Article number	6113
Journal	Scientific Reports
Volume	7
Issue number	1
DOIs	https://doi.org/10.1038/s41598-017-06124-z
State	Published - Dec 1 2017

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title = "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 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.",

author = "Mengmeng Zhao and Yongguang Hu and Jiayi Jin and Ying Yu and Shanshan Zhang and Jingjing Cao and Yuanfen Zhai and Rongbin Wei and Juanjuan Shou and Wenping Cai and Shangfeng Liu and Xiaoping Yang and Xu, {Guo Tong} and Jianhua Yang and Corry, {David B.} and Su, {Shao Bo} and Xialin Liu and Tianshu Yang",

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doi = "10.1038/s41598-017-06124-z",

language = "English (US)",

volume = "7",

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T1 - Interleukin 37 promotes angiogenesis through TGF-β signaling

AU - Zhao, Mengmeng

AU - Hu, Yongguang

AU - Jin, Jiayi

AU - Yu, Ying

AU - Zhang, Shanshan

AU - Cao, Jingjing

AU - Zhai, Yuanfen

AU - Wei, Rongbin

AU - Shou, Juanjuan

AU - Cai, Wenping

AU - Liu, Shangfeng

AU - Yang, Xiaoping

AU - Xu, Guo Tong

AU - Yang, Jianhua

AU - Corry, David B.

AU - Su, Shao Bo

AU - Liu, Xialin

AU - Yang, Tianshu

PY - 2017/12/1

Y1 - 2017/12/1

N2 - 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.

AB - 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.

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VL - 7

JO - Scientific Reports

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Interleukin 37 promotes angiogenesis through TGF-β signaling

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