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1.
Figure 2

Figure 2. Summary of potential differential effects of PTH signaling in the HSC niche. From: Communications between bone cells and hematopoietic stem cells.

Signaling through the PTH1R on osteoblasts causes an increased production in RANKL, which in turn recruits osteoclasts (gray cell). PTH also increases CXCL12 which can interact with CXCR4 on HSC. Jagged1 expression is upregulated with PTH1R stimulation, which activates Notch signaling in the HSC. Prostaglandin E2 production also increases with PTH signaling, mostly through upregulation of COX-2. Osteopontin (OPN) produced by osteoblasts interacts with receptors on HSC and negatively regulates the number of HSC in the niche.

R.L. Porter, et al. Arch Biochem Biophys. ;473(2):193-200.
2.
Figure 1

Figure 1. Summary of the major signaling pathways involved in regulating self-renewal and differentiation of HSC. From: Communications between bone cells and hematopoietic stem cells.

PTH signaling through the PTH1R on osteoblasts (blue cell) acts via PKA and PLC to increase expression of the Notch ligand Jagged1, which can then interact with Notch receptors on HSC (tan cell). Notch signaling within the HSC causes cleavage of the Notch intracellular domain (NICD) which translocates to the nucleus and results in self-renewal of the HSC. Wnt proteins produced by osteoblasts interact with receptors on HSC such as Frizzled and LPR5 and also induce self-renewal via β-catenin. In contrast to these self-renewal signals, BMP signaling in osteoblasts is thought to indirectly inhibit proliferation of HSC by limiting the niche cells available to support HSC.

R.L. Porter, et al. Arch Biochem Biophys. ;473(2):193-200.

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