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Myeloid cells protect intestinal epithelial barrier integrity through the angiogenin/plexin‐B2 axis
Author(s) -
Bai Rongpan,
Sun Desen,
Chen Muxiong,
Shi Xiaoliang,
Luo Liang,
Yao Zhengrong,
Liu Yaxin,
Ge Xiaolong,
Gao Xiangwei,
Hu Guofu,
Zhou Wei,
Sheng Jinghao,
Xu Zhengping
Publication year - 2020
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.2019103325
Subject(s) - china , family medicine , medicine , traditional chinese medicine , library science , cancer , traditional medicine , alternative medicine , political science , pathology , law , computer science
Communication between myeloid cells and epithelium plays critical role in maintaining intestinal epithelial barrier integrity. Myeloid cells interact with intestinal epithelial cells ( IEC s) by producing various mediators; however, the molecules mediating their crosstalk remain incompletely understood. Here, we report that deficiency of angiogenin ( Ang ) in mouse myeloid cells caused impairment of epithelial barrier integrity, leading to high susceptibility to DSS ‐induced colitis. Mechanistically, myeloid cell‐derived angiogenin promoted IEC survival and proliferation through plexin‐B2‐mediated production of tRNA ‐derived stress‐induced small RNA (ti RNA ) and transcription of ribosomal RNA ( rRNA ), respectively. Moreover, treatment with recombinant angiogenin significantly attenuated the severity of experimental colitis. In human samples, the expression of angiogenin was significantly down‐regulated in patients with inflammatory bowel disease ( IBD ). Collectively, we identified, for the first time to our knowledge, a novel mediator of myeloid cell‐ IEC crosstalk in maintaining epithelial barrier integrity, suggesting that angiogenin may serve as a new preventive agent and therapeutic target for IBD.