Here, we demonstrated that Phd1 deletion in endothelial and haematopoietic cells (Phd1<sup>f/</sup><sup>f</sup> Tie2:cre) protected mice from dextran sulphate sodium (DSS)-induced colitis, with reduced epithelial erosions, immune cell infiltration, and colonic microvascular dysfunction, whereas the response of Phd2<sup>f/+</sup> Tie2:cre and Phd3<sup>f/</sup><sup>f</sup> Tie2:cre mice to DSS was similar to that of their littermate controls.
Reduced susceptibility of PHD1(-/-) mice to colitis was associated with increased density of colonic epithelial cells relative to wild-type controls, which was because of decreased levels of apoptosis that resulted in enhanced epithelial barrier function.