Bone Marrow Research (NK) cells by producing prostaglandin E2 (PGE2), a product of arachidonic acid metabolism that acts as a powerful immune suppressant, and inhibits T-cell mitogenesis and IL- 2 production [88, 97, 98] (Figure 1). 5. Conclusion Lines of evidence have indicated that MSCs are capable of supporting the expansion and diﬀerentiation of HSCs and enhancing hematopoietic engraftment in the past two decades, but the exact mechanisms by how MSCs support HSCs are still unclear. MSCs may aﬀect HSCs by producing growth factors and chemokines that take parts in signaling pathways regulating HSCs. Meanwhile, HSCs interact with MSCs though this has been less understood. MSCs can home to injured tissues when coinfused with HSCs [99]. A better understanding of the interaction between MSCs and HSCs will substantially ultimately help develop novel therapies for hematopoietic diseases. Acknowledgment This paper was supported by grants from Natural Sci- ence Foundation of China (nos. 30871273, 30971496, and U1032003) and from Shenzhen (JC201005280597A) to Y. Wu. References [1] S. H. Orkin and L. I. Zon, “Hematopoiesis: an evolving paradigm for stem cell biology,” Cell, vol. 132, no. 4, pp. 631– 644, 2008. [2] Group SCTC, “Allogeneic peripheral blood stem-cell com- pared with bone marrow transplantation in the management of hematologic malignancies: an individual patient data meta-analysis of nine randomized trials,” Journal of Clinical Oncology, vol. 23, no. 22, pp. 5074–5087, 2005. [3] L. Murray, B. Chen, A. Galy et al., “Enrichment of human hematopoietic stem cell activity in the CD34+Thy- 1+Lin subpopulation from mobilized peripheral blood,” Blood, vol. 85, no. 2, pp. 368–378, 1995. [4] N. Flomenberg, S. M. Devine, J. F. DiPersio et al., “The use of AMD3100 plus G-CSF for autologous hematopoietic progenitor cell mobilization is superior to G-CSF alone,” Blood, vol. 106, no. 5, pp. 1867–1874, 2005. [5] E. Gluckman, H. A. Broxmeyer, A. D. Auerbach et al., “Hematopoietic reconstitution in a patient with Fanconi’s anemia by means of umbilical-cord blood from an HLA- identical sibling,” New England Journal of Medicine, vol. 321, no. 17, pp. 1174–1178, 1989. [6] L. Pierelli, G. Scambia, G. Bonanno et al., “CD34+/CD105+ cells are enriched in primitive circulating progenitors residing in the G0 phase of the cell cycle and contain all bone marrow and cord blood CD34+/CD38low/− precursors,” British Journal of Haematology, vol. 108, no. 3, pp. 610–620, 2000. [7] S. J. Morrison and A. C. Spradling, “Stem cells and niches: mechanisms that promote stem cell maintenance throughout life,” Cell, vol. 132, no. 4, pp. 598–611, 2008. [8] L. M. Calvi, G. B. Adams, K. W. Weibrecht et al., “Osteoblastic cells regulate the haematopoietic stem cell niche,” Nature, vol. 425, no. 6960, pp. 841–846, 2003. 5 [9] J. W. Zhang, C. Niu, L. Ye et al., “Identiﬁcation of the haematopoietic stem cell niche and control of the niche size,” Nature, vol. 425, no. 6960, pp. 836–841, 2003. [10] S. Me´ndez-Ferrer, D. Lucas, M. Battista, and P. S. Frenette, “Haematopoietic stem cell release is regulated by circadian oscillations,” Nature, vol. 452, no. 7186, pp. 442–447, 2008. [11] T. Sugiyama, H. Kohara, M. Noda, and T. Nagasawa, “Mainte- nance of the hematopoietic stem cell pool by CXCL12-CXCR4 chemokine signaling in bone marrow stromal cell niches,” Immunity, vol. 25, no. 6, pp. 977–988, 2006. [12] M. Scheller, J. Huelsken, F. Rosenbauer et al., “Hematopoietic stem cell and multilineage defects generated by constitutive β-catenin activation,” Nature Immunology, vol. 7, no. 10, pp. 1021–1023, 2006. [13] T. Suda and F. Arai, “Wnt signaling in the niche,” Cell, vol. 132, no. 5, pp. 729–730, 2008. [14] H. E. Fleming, V. Janzen, C. L. Celso et al., “Wnt signaling in the niche enforces hematopoietic stem cell quiescence and is necessary to preserve self-renewal in vivo,” Cell Stem Cell, vol. 2, no. 3, pp. 274–283, 2008. [15] P. Eliasson and J. Jo¨nsson, “The hematopoietic stem cell niche: low in oxygen but a nice place to be,” Journal of Cellular Physiology, vol. 222, no. 1, pp. 17–22, 2010. [16] K. Hosokawa, F. Arai, H. Yoshihara et al., “Function of oxidative stress in the regulation of hematopoietic stem cell-niche interaction,” Biochemical and Biophysical Research Communications, vol. 363, no. 3, pp. 578–583, 2007. [17] M. F. Pittenger and B. J. Martin, “Mesenchymal stem cells and their potential as cardiac therapeutics,” Circulation Research, vol. 95, no. 1, pp. 9–20, 2004. [18] M. Valtieri and A. Sorrentino, “The mesenchymal stromal cell contribution to homeostasis,” Journal of Cellular Physiology, vol. 217, no. 2, pp. 296–300, 2008. [19] G. Ko¨gler, S. Sensken, J. A. Airey et al., “A new human somatic stem cell from placental cord blood with intrinsic pluripotent diﬀerentiation potential,” Journal of Experimental Medicine, vol. 200, no. 2, pp. 123–135, 2004. [20] T. Tondreau, L. Lagneaux, M. Dejeneﬂe et al., “Bone marrow- derived mesenchymal stem cells already express speciﬁc neural proteins before any diﬀerentiation,” Diﬀerentiation, vol. 72, no. 7, pp. 319–326, 2004. [21] J. E. Dennis and P. Charbord, “Origin and diﬀerentiation of human and murine stroma,” Stem Cells, vol. 20, no. 3, pp. 205– 214, 2002. [22] M. Dominici, K. Le Blanc, I. Mueller et al., “Minimal criteria for deﬁning multipotent mesenchymal stromal cells. The International Society for Cellular Therapy position state- ment,” Cytotherapy, vol. 8, no. 4, pp. 315–317, 2006. [23] E. Imai and T. Ito, “Can bone marrow diﬀerentiate into renal cells?” Pediatric Nephrology, vol. 17, no. 10, pp. 790–794, 2002. [24] S. T. Mohanty, L. Kottam, A. Gambardella et al., “Alterations in the self-renewal and diﬀerentiation ability of bone marrow mesenchymal stem cells in a mouse model of rheumatoid arthritis,” Arthritis Research and Therapy, vol. 12, no. 4, p. R149, 2010. [25] O. N. Koc¸, S. L. Gerson, B. W. Cooper et al., “Rapid hematopoietic recovery after coinfusion of autologous-blood stem cells and culture-expanded marrow mesenchymal stem cells in advanced breast cancer patients receiving high-dose chemotherapy,” Journal of Clinical Oncology, vol. 18, no. 2, pp. 307–316, 2000. [26] K. L. Blanc, I. Rasmusson, B. Sundberg et al., “Treatment of severe acute graft-versus-host disease with third party