Myeloid cells protect intestinal epithelial barrier integrity through the angiogenin/plexin-B2 axis
Myeloid cells protect intestinal epithelial barrier integrity through the angiogenin/plexin-B2 axis
复制标题
骨髓细胞通过血管生成素/丛蛋白-B2 轴保护肠上皮屏障完整性
DOI：
10.15252/embj.2019103325
复制
发表时间：
2020-06-08
期刊：
影响因子：
11.4
通讯作者：
Xu, Zhengping
中科院分区：
文献类型：
--
作者：
Bai, Rongpan;Sun, Desen;Xu, Zhengping
Communication between myeloid cells and epithelium plays critical role in maintaining intestinal epithelial barrier integrity. Myeloid cells interact with intestinal epithelial cells (IECs) 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 (tiRNA) 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.
