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Wu, Ningbo; Sun, Hongxiang; Zhao, Xiaoyun; Zhang, Yao; Tan, Jianmei; Qi, Yuanyuan; Wang, Qun; Ng, Melissa; Liu, Zhaoyuan; He, Lingjuan; Niu, Xiaoyin; Chen, Lei; Liu, Zhiduo; Li, Hua-Bing; Zeng, Yi Arial; Roulis, Manolis; Liu, Dou; Cheng, Jinke; Zhou, Bin; Ng, Lai Guan; Zou, Duowu; Ye, Youqiong; Flavell, Richard A; Ginhoux, Florent; Su, Bing
Nature (London), 04/2021, Letnik: 592, Številka: 7855Journal Article
Intestinal stromal cells are known to modulate the propagation and differentiation of intestinal stem cells . However, the precise cellular and molecular mechanisms by which this diverse stromal cell population maintains tissue homeostasis and repair are poorly understood. Here we describe a subset of intestinal stromal cells, named MAP3K2-regulated intestinal stromal cells (MRISCs), and show that they are the primary cellular source of the WNT agonist R-spondin 1 following intestinal injury in mice. MRISCs, which are epigenetically and transcriptomically distinct from subsets of intestinal stromal cells that have previously been reported , are strategically localized at the bases of colon crypts, and function to maintain LGR5 intestinal stem cells and protect against acute intestinal damage through enhanced R-spondin 1 production. Mechanistically, this MAP3K2 specific function is mediated by a previously unknown reactive oxygen species (ROS)-MAP3K2-ERK5-KLF2 axis to enhance production of R-spondin 1. Our results identify MRISCs as a key component of an intestinal stem cell niche that specifically depends on MAP3K2 to augment WNT signalling for the regeneration of damaged intestine.
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