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Here, we demonstrate that Periostin (Postn) via interaction with Integrin-\u03b1v (Itgav) regulates HSC proliferation. Systemic deletion of Postn results in peripheral blood (PB) anaemia, myelomonocytosis and lymphopenia, while the number of phenotypic HSCs increases in the bone marrow.\n                    <jats:italic>Postn<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice recover faster from radiation injury with concomitant loss of primitive HSCs. HSCs from\n                    <jats:italic>Postn<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    mice show accumulation of DNA damage generally associated with aged HSCs. Itgav deletion in the haematopoietic system leads to a similar PB phenotype and HSC-intrinsic repopulation defects. Unaffected by Postn,\n                    <jats:italic>Vav-Itgav<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>\u2212\/\u2212<\/jats:italic>\n                    <\/jats:sup>\n                    HSCs proliferate faster\n                    <jats:italic>in vitro<\/jats:italic>\n                    , illustrating the importance of Postn-Itgav interaction. Finally, the Postn-Itgav interaction inhibits the FAK\/PI3K\/AKT pathway in HSCs, leading to increase in p27Kip1 expression resulting in improved maintenance of quiescent HSCs. Together, we demonstrate a role for Itgav-mediated outside-in signalling in regulation of HSC proliferation and stemness.\n                  <\/jats:p>","DOI":"10.1038\/ncomms13500","type":"journal-article","created":{"date-parts":[[2016,12,1]],"date-time":"2016-12-01T05:08:56Z","timestamp":1480568936000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":81,"title":["Outside-in integrin signalling regulates haematopoietic stem cell function via Periostin-Itgav axis"],"prefix":"10.1038","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5176-1510","authenticated-orcid":false,"given":"Satish","family":"Khurana","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Schouteden","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Javed K.","family":"Manesia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albert","family":"Santamaria-Mart\u00ednez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joerg","family":"Huelsken","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam","family":"Lacy-Hulbert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine M.","family":"Verfaillie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2016,12,1]]},"reference":[{"key":"BFncomms13500_CR1","doi-asserted-by":"crossref","first-page":"11","DOI":"10.1038\/nrm2319","volume":"9","author":"DL Jones","year":"2008","unstructured":"Jones, D. 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