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Blood, 1 July 2007, Vol. 110, No. 1, pp. 82-90.
Prepublished online as a Blood First Edition Paper on March 14, 2007; DOI 10.1182/blood-2006-05-021352.
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Submitted May 5, 2006
Accepted February 28, 2007
Annexin II expressed by osteoblasts & endothelial cells
regulates stem cell adhesion, homing & engraftment
following transplantation
Younghun Jung, Jingcheng Wang, Junhui Song, Yusuke Shiozawa, Jianhua Wang, Aaron Havens, Zhuo Wang, Yan-Xi Sun, Stephen G. Emerson, Paul H Krebsbach, and Russell S Taichman*
Dept of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI
Dept of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI
Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA
* Corresponding author; email: rtaich{at}umich.edu.
Differentiation of hematopoietic stem cells (HSCs) after birth is largely restricted to the bone marrow cavity, where HSCs are associated closely with osteoblasts (OBs). How OBs localize HSCs to the endosteal niche remains unclear. To explore adhesive interactions between HSCs and OBs, a cell blot analysis was used which revealed two major bands that corresponded to monomers and multimers of annexin II (AXII). Immunohistochemistry revealed that OBs and marrow endothelial cells express AXII at high levels. Function-blocking studies confirmed that AXII mediates HSCs adhesion mainly via the N-terminal portion of the AXII peptide. Adhesion of HSCs to OBs derived from AXII deficient animals (AXII-/-) was significantly impaired compared to OBs obtained from wild-type animals (AXII+/+). Moreover, fewer HSCs were found in the marrow of AXII-/- vs AXII+/+ animals. Short-term lodging, engraftment and survival of irradiated mice with whole marrow cells were substantially inhibited by N-terminal peptide fragments of AXII or anti-AXII antibodies. Similar findings were noted in long term competitive repopulation studies. Collectively, these findings reveal that AXII regulates HSC homing and binding to the bone marrow microenvironment and suggest that AXII is crucial for determining the bone marrow niche of HSCs.
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