<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sa da Bandeira D</submitter><funding>British Heart Foundation</funding><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><funding>Academy of Medical Sciences</funding><pagination>111114</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9638014</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(3)</volume><pubmed_abstract>Hematopoietic stem cell (HSC) generation in the aorta-gonad-mesonephros region requires HSC specification signals from the surrounding microenvironment. In zebrafish, PDGF-B/PDGFRβ signaling controls hematopoietic stem/progenitor cell (HSPC) generation and is required in the HSC specification niche. Little is known about murine HSPC specification in vivo and whether PDGF-B/PDGFRβ is involved. Here, we show that PDGFRβ is expressed in distinct perivascular stromal cell layers surrounding the mid-gestation dorsal aorta, and its deletion impairs hematopoiesis. We demonstrate that PDGFRβ&lt;sup>+&lt;/sup> cells play a dual role in murine hematopoiesis. They act in the aortic niche to support HSPCs, and in addition, PDGFRβ&lt;sup>+&lt;/sup> embryonic precursors give rise to a subset of HSPCs that persist into adulthood. These findings provide crucial information for the controlled production of HSPCs in vitro.</pubmed_abstract><journal>Cell reports</journal><pubmed_title>PDGFRβ&lt;sup>+&lt;/sup> cells play a dual role as hematopoietic precursors and niche cells during mouse ontogeny.</pubmed_title><pmcid>PMC9638014</pmcid><funding_grant_id>219542/Z/19/Z</funding_grant_id><funding_grant_id>RE/18/5/34216</funding_grant_id><funding_grant_id>SBF001\1007</funding_grant_id><funding_grant_id>RM/17/3/33381</funding_grant_id><pubmed_authors>Rossi F</pubmed_authors><pubmed_authors>van der Linden R</pubmed_authors><pubmed_authors>Sa da Bandeira D</pubmed_authors><pubmed_authors>Vink CS</pubmed_authors><pubmed_authors>Beltran M</pubmed_authors><pubmed_authors>Vermeren M</pubmed_authors><pubmed_authors>Henderson NC</pubmed_authors><pubmed_authors>Gonzalez ZN</pubmed_authors><pubmed_authors>Jung B</pubmed_authors><pubmed_authors>van de Werken HJG</pubmed_authors><pubmed_authors>Forbes SJ</pubmed_authors><pubmed_authors>Kilpatrick AM</pubmed_authors><pubmed_authors>Stefancova D</pubmed_authors><pubmed_authors>van Ijcken WFJ</pubmed_authors><pubmed_authors>Crisan M</pubmed_authors><pubmed_authors>Ventura T</pubmed_authors><pubmed_authors>Gomez-Salazar M</pubmed_authors><pubmed_authors>Marques M</pubmed_authors><pubmed_authors>Betsholtz C</pubmed_authors><pubmed_authors>Cuervo H</pubmed_authors></additional><is_claimable>false</is_claimable><name>PDGFRβ&lt;sup>+&lt;/sup> cells play a dual role as hematopoietic precursors and niche cells during mouse ontogeny.</name><description>Hematopoietic stem cell (HSC) generation in the aorta-gonad-mesonephros region requires HSC specification signals from the surrounding microenvironment. In zebrafish, PDGF-B/PDGFRβ signaling controls hematopoietic stem/progenitor cell (HSPC) generation and is required in the HSC specification niche. Little is known about murine HSPC specification in vivo and whether PDGF-B/PDGFRβ is involved. Here, we show that PDGFRβ is expressed in distinct perivascular stromal cell layers surrounding the mid-gestation dorsal aorta, and its deletion impairs hematopoiesis. We demonstrate that PDGFRβ&lt;sup>+&lt;/sup> cells play a dual role in murine hematopoiesis. They act in the aortic niche to support HSPCs, and in addition, PDGFRβ&lt;sup>+&lt;/sup> embryonic precursors give rise to a subset of HSPCs that persist into adulthood. These findings provide crucial information for the controlled production of HSPCs in vitro.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jul</publication><modification>2024-11-10T02:22:39.247Z</modification><creation>2024-11-10T02:22:39.247Z</creation></dates><accession>S-EPMC9638014</accession><cross_references><pubmed>35858557</pubmed><doi>10.1016/j.celrep.2022.111114</doi></cross_references></HashMap>