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FOXC1 and FOXC2 promote endothelial-derived R-spondin 3 and CXCL12 signals in intestinal regeneration after ischemia-reperfusion injury

ABSTRACT: Intestinal ischemia induces mucosal damage while simultaneously activating intestinal stem cells (ISCs), which subsequently regenerate the damaged intestinal epithelium. However, whether angiocrine factors secreted from vascular endothelial cells (ECs) - blood and lymphatic ECs (BECs and LECs, respectively) – regulate ISC-mediated regeneration have yet to be elucidated. Here, we identify FOXC1 and FOXC2 as essential regulators of angiocrine signaling in regeneration of the small intestine after ischemia-reperfusion (I/R) injury. EC- and LEC-specific deletions of Foxc1, Foxc2, or both in mice augment I/R-induced intestinal damage by causing defects in vascular regrowth, expression of the chemokine CXCL12 and the Wnt activator R-spondin 3 in BECs and LECs, respectively, and activation of Wnt signaling in ISCs. Treatment with CXCL12 and R-spondin 3 rescues the I/R-induced intestinal damage in EC- and LEC-Foxc mutant mice, respectively. This study provides evidence that FOXC1 and FOXC2 are required for intestinal regeneration by stimulating angiocrine CXCL12 and Wnt signaling.

ORGANISM(S): Mus musculus

PROVIDER: GSE190581 | GEO | 2021/12/13

REPOSITORIES: GEO

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FOXC1 and FOXC2 promote endothelial-derived R-spondin 3 and CXCL12 signals in intestinal regeneration after ischemia-reperfusion injury

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