Abstract
Increasing evidence suggest functional roles of subepithelial mesenchymal niche cells in maintaining intestinal stem cells and in modulating the pathogenesis of various intestinal diseases in mammals. A recent study reported the discovery of a new population of stromal cells in mice termed MAP3K2-Regulated Intestinal Stromal Cells (MRISCs); these cells reside at the base of colonic crypt and function to protect colonic stem cells during colonic inflammation by expressing the Wnt agonist R-spondin1 (Rspo1).
Highlights
The epithelium that lines the mammalian intestinal and colonic tube is continuously renewed with the progenies of stem cells that reside at the bottom of an invaginated structure termed the crypt
That study began with a phenotypic analysis of mice deficient for Map3k2, a serine/threonine kinase belonging to the mitogen-activated protein kinase kinase kinase (MAP3K) superfamily that has been implicated in cellular stress responses. They observed that Map3k2−/− mice exhibited an enhanced colitis phenotype, with a significantly reduced number of colonic stem cells present following exposure to dextran sulfate sodium (DSS)
It is notable that scRNA-seq and ATACseq analyses revealed that MAP3K2-Regulated Intestinal Stromal Cells (MRISCs) appear to be epigenetically and transcriptionally distinct from other subpopulations of intestinal stromal cells, including telocytes, trophocytes, and Ptgs2-expressing fibroblasts (Degirmenci et al 2018; McCarthy et al 2020b; Roulis et al 2020; Shoshkes-Carmel et al 2018)
Summary
The epithelium that lines the mammalian intestinal and colonic tube is continuously renewed with the progenies of stem cells that reside at the bottom of an invaginated structure termed the crypt. They observed that Map3k2−/− mice exhibited an enhanced colitis phenotype, with a significantly reduced number of colonic stem cells present following exposure to dextran sulfate sodium (DSS). The Col1a2-creERT2; Map3k2fl/fl mice (Map3k2 is ablated in the subepithelial stromal cells) developed a severe colitis phenotype similar to the Map3k2−/− mice.
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