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Sci Rep. 2017 Jul 21;7(1):6113. doi: 10.1038/s41598-017-06124-z.

Interleukin 37 promotes angiogenesis through TGF-β signaling.

Author information

1
Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
2
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
3
Johns Hopkins University School of Medicine, Baltimore, United States.
4
Department of Pathology and Immunology, Baylor College of Medicine, Houston, United States.
5
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China. liuxl28@mail.sysu.edu.cn.
6
Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China. tianshuy@tongji.edu.cn.

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.

PMID:
28733640
PMCID:
PMC5522482
DOI:
10.1038/s41598-017-06124-z
[Indexed for MEDLINE]
Free PMC Article

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