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Interleukin 37 promotes angiogenesis through TGF-β signaling.

Interleukin 37 promotes angiogenesis through TGF-β signaling.
Author Information (click to view)

Zhao M, Hu Y, Jin J, Yu Y, Zhang S, Cao J, Zhai Y, Wei R, Shou J, Cai W, Liu S, Yang X, Xu GT, Yang J, Corry DB, Su SB, Liu X, Yang T,


Zhao M, Hu Y, Jin J, Yu Y, Zhang S, Cao J, Zhai Y, Wei R, Shou J, Cai W, Liu S, Yang X, Xu GT, Yang J, Corry DB, Su SB, Liu X, Yang T, (click to view)

Zhao M, Hu Y, Jin J, Yu Y, Zhang S, Cao J, Zhai Y, Wei R, Shou J, Cai W, Liu S, Yang X, Xu GT, Yang J, Corry DB, Su SB, Liu X, Yang T,

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Scientific reports 2017 07 217(1) 6113 doi 10.1038/s41598-017-06124-z
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.

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