Figure 1.

HSCs can be regulated through activation of various signaling molecules and cell types. A, Circadian rhythms can activate SNS neurons to release catecholamines that can act directly on HSCs but also inhibit CAR cell production of CXCL12, facilitating HSC egress (18, 78). B, PTH stimulation activates T cells to produce Wnt10b, which stimulates HSC support directly and also through activating osteoblasts (53, 79). Wnt10b stimulation also inhibits adipogenesis, an effect which may decrease an inhibitory HSC niche component (B) (47–51). C, Estrogen has been shown to have opposing effects on the hematopoietic system, including inhibiting T lymphocytes, but can also expand HSCs expressing estrogen receptor-α (ERα) (85, 87). D, PGE2 can stimulate HSC support both autonomously and cell nonautonomously by activating GαS on MSCs (89, 92).