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. 2019 Mar 12;7:34. doi: 10.3389/fcell.2019.00034

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Copyright © 2019 Mahony and Bertrand.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Summary of vertebrate HSC expansion in the embryonic niche. Following their derivation from aortic endothelium, HSCs home to their embryonic niche in response to several attractive cytokines, such as cxcl12 and ccl25b/Ccl21. HSCs are directed toward vascular cells by Mφ (macrophages). The vascular cells in the embryonic niche then remodel to accommodate the arriving HSCs. HSCs then become lodged in the fetal niche and undergo cell division to expand their initial number. This expansion is in response to several cytokines released from many different cell types. Endothelial cells release kitlg and osm, under the control of tfec. Stromal cells release cxcl12, under the control of atf4. Hepatoblasts release Kit-ligand and angiopoietins. After considerable expansion, the ECM is remodeled by Mmp9 released from neutrophils and HSCs leave their fetal niche to migrate to their adult niche. Outlined here is an overview of the main cell types involved in fetal HSC expansion along with some examples of important cytokines/signals that they secrete, although many others exist.