当前位置: X-MOL 学术J. Exp. Med. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Sensing of apoptotic cells through Axl causes lung basal cell proliferation in inflammatory diseases.
Journal of Experimental Medicine ( IF 15.3 ) Pub Date : 2019-07-09 , DOI: 10.1084/jem.20171978
Naoya Fujino 1, 2 , Oliver J Brand 3, 4 , David J Morgan 3, 4 , Toshifumi Fujimori 3 , Aleksander M Grabiec 3, 5 , Christopher P Jagger 3, 4 , Rose A Maciewicz 6, 7 , Mitsuhiro Yamada 2 , Koji Itakura 2 , Hisatoshi Sugiura 2 , Masakazu Ichinose 2 , Tracy Hussell 1, 4
Affiliation  

Epithelial cell proliferation, division, and differentiation are critical for barrier repair following inflammation, but the initial trigger for this process is unknown. Here we define that sensing of apoptotic cells by the TAM receptor tyrosine kinase Axl is a critical indicator for tracheal basal cell expansion, cell cycle reentry, and symmetrical cell division. Furthermore, once the pool of tracheal basal cells has expanded, silencing of Axl is required for their differentiation. Genetic depletion of Axl triggers asymmetrical cell division, leading to epithelial differentiation and ciliated cell regeneration. This discovery has implications for conditions associated with epithelial barrier dysfunction, basal cell hyperplasia, and continued turnover of dying cells in patients with chronic inflammatory pulmonary diseases.

中文翻译:

通过 Axl 感知凋亡细胞会导致炎症性疾病中的肺基底细胞增殖。

上皮细胞增殖、分裂和分化对于炎症后的屏障修复至关重要,但这一过程的初始触发因素尚不清楚。在这里,我们定义 TAM 受体酪氨酸激酶 Axl 对凋亡细胞的感知是气管基底细胞扩增、细胞周期折返和对称细胞分裂的关键指标。此外,一旦气管基底细胞库扩大,Axl 的沉默是其分化所必需的。Axl 的基因缺失触发不对称细胞分裂,导致上皮分化和纤毛细胞再生。这一发现对慢性炎症性肺病患者与上皮屏障功能障碍、基底细胞增生和垂死细胞持续更新相关的疾病有影响。
更新日期:2019-09-03
down
wechat
bug