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 Blood, 15 February 2008, Vol. 111, No. 4, pp. 2436-2443.
Prepublished online as a Blood First Edition Paper on November 28, 2007; DOI 10.1182/blood-2007-07-099333.

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Submitted July 12, 2007
Accepted November 23, 2007

Identification of mesenchymal stem cells in aorta-gonad-mesonephros and yolk sac of human embryos

Xiao-Yan Wang, Yu Lan, Wen-Yan He, Lei Zhang, Hui-Yu Yao, Chun-Mei Hou, Ying Tong, Yuan-Lin Liu, Guan Yang, Xiao-Dan Liu, Xiao Yang, Bing Liu, and Ning Mao*

Department of Cell Biology, Institute of Basic Medical Sciences, Beijing, China
Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing, China
Department of Gynecology and Obstetrics, Air Force General Hospital, Beijing, China

* Corresponding author; email: maoning{at}nic.bmi.ac.cn.

Mesenchymal stem cells (MSCs) are multi-potent stem cells that can generate various microenvironment components in bone marrow, ensuring a precise control over self-renewal and multi-lineage differentiation of hematopoietic stem cells. Nevertheless, their spatiotemporal correlation with embryonic hematopoiesis remains rudimentary, particularly in relation to the human being. Here, we reported that human aorta-gonad-mesonephros (AGM) resided with bona fide MSCs. They were highly proliferative as fibroblastoid population bearing uniform surface markers (CD45-, CD34-, CD105+, CD73+, CD29+, and CD44+), expressed pluri-potential molecules Oct-4 and Nanog, and clonally demonstrated tri-lineage differentiation capacity (osteocytes, chondrocytes and adipocytes). The frequency and absolute number of MSCs in aorta plus surrounding mesenchyme (E26-27) were 0.3% and 164 respectively. Moreover, they were functionally equivalent to MSCs from adult bone marrow, i.e., supporting long-term hematopoiesis and suppressing T lymphocyte proliferation in vitro. In comparison, the matching yolk sac contained bi-potent mesenchymal precursors that propagated more slowly and failed to generate chondrocytes in vitro. Together with previous knowledge, we propose that a proportion of MSCs initially develop in human AGM prior to their emergence in embryonic circulation and fetal liver.


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