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We have used an in vitro embryonic stem (ES) cell culture system to prepare endothelial progenitor cells (EPC) lacking PS1 and investigated the roles of PS1 in endothelial cell lineage. With this system, Flk\u20101<jats:sup>+<\/jats:sup> E\u2010cadherin<jats:sup>\u2212<\/jats:sup> EPC were generated from PS1\u2010deficient ES cells, and the EPC lacking PS1 as well as wild\u2010type EPC grew to form VE\u2010cadherin<jats:sup>+<\/jats:sup> endothelial colonies supported by a layer of OP9 stromal cells. Although the endothelial colonies from PS1\u2010deficient EPC showed morphology similar to those from wild\u2010type EPC, the PS1\u2010deficient EPC formed a large number of the colonies compared to wild\u2010type EPC. The enhanced colony\u2010forming ability of PS1\u2010deficient EPC was attenuated by the inductions of wild\u2010type human PS1. To differentiate multiple activities of PS1 for colony\u2010forming ability, we used two types of human PS1 mutants: one (hPS1D257A) with the aspartate to alanine mutation at residue 257 that impairs the proteolytic activity of PS1, and the other (hPS1\u0394cat) deleting amino acids 340\u2013371 of the cytosolic loop sequence essential for \u03b2\u2010catenin binding. hPS1D257A showed activity to regulate the colony\u2010forming ability of PS1\u2010deficient EPC, while hPS1\u0394cat failed to exhibit this activity. These results suggest that PS1 regulates the growth and differentiation of endothelial progenitor cells through its \u03b2\u2010catenin\u2010binding region and that the defect of PS1 function in endothelial cell lineage could contribute to the induction of vascular pathology.<\/jats:p>","DOI":"10.1016\/j.cellbi.2005.11.003","type":"journal-article","created":{"date-parts":[[2005,12,23]],"date-time":"2005-12-23T12:14:01Z","timestamp":1135340041000},"page":"239-243","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Presenilin\u20101 controls the growth and differentiation of endothelial progenitor cells through its \u03b2\u2010catenin\u2010binding 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