After DNA damage, AREG-ular niche it's not

In this issue of Blood, Wu et al(1) have demonstrated that leptin receptor-expressing (LepR(+)) bone marrow (BM) stromal cells upregulate and secrete amphiregulin (AREG) in mice during aging and in mice deficient in the DNA repair gene Brca2. This increase in AREG promotes a decline in hematopoietic stem cell (HSC) repopulating capacity. In the current paradigm of hematopoiesis, niche-derived paracrine growth factors, such as stem cell factor, CXCL12, and pleiotrophin,(2-4) provide essential support for HSC maintenance. The study by Wu et al adds importantly to this paradigm by demonstrating the contribution of a niche-derived paracrine factor in pathologic conditions, such as genotoxic injury, or during aging.