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Migration of dorsal aorta mesenchymal stem cells induced by mouse embryonic circulation
Author(s) -
Yan XinLong,
Lan Yu,
Wang XiaoYan,
He WenYan,
Yao HuiYu,
Chen DongBo,
Xiong JiaXiang,
Gao Jiao,
Li Zhuan,
Yang Guan,
Li XiuSen,
Liu YuanLin,
Zhang JiYan,
Liu Bing,
Mao Ning
Publication year - 2011
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22490
Subject(s) - biology , microbiology and biotechnology , mesenchymal stem cell , dorsal aorta , embryonic stem cell , hemangioblast , stem cell , immunology , haematopoiesis , genetics , gene
Mesenchymal stem cells (MSCs) represent powerful tools for regenerative medicine for their differentiation and migration capacity. However, ontogeny and migration of MSCs in mammalian mid‐gestation conceptus is poorly understood. We identified canonical MSCs in the mouse embryonic day (E) 11.5 dorsal aorta (DA). They possessed homogenous immunophenotype (CD45 − CD31 − Flk‐1 − CD44 + CD29 + ), expressed perivascular markers (α‐SMA + NG2 + PDGFRβ + PDGFRα + ), and had tri‐lineage differentiation potential (osteoblasts, adipocytes, and chondrocytes). Of interest, MSCs were also detected in E12.5–E13.5 embryonic circulation, 24 hr later than in DA, suggesting migration like hematopoietic stem cells. Functionally, E12.5 embryonic blood could trigger efficient migration of DA‐MSCs through platelet‐derived growth factor (PDGF) receptor‐, transforming growth factor‐beta receptor‐, but not basic fibroblast growth factor receptor‐mediated signaling. Moreover, downstream JNK and AKT signaling pathway played important roles in embryonic blood‐ or PDGF‐mediated migration of DA‐derived MSCs. Taken together, these results revealed that clonal MSCs developed in the mouse DA. More importantly, the embryonic circulation, in addition to its conventional transporting roles, could modulate migration of MSC during early embryogenesis. Developmental Dynamics, 2011. © 2010 Wiley‐Liss, Inc.