Adhesion Molecules in Stem Cells - Adhesion Molecules - page 123

Table 1 Cell surface markers of MSCs

Positive Negative or very low expression

Adhesion molecules CD44, CD73, CD105, PECAM-1, L-selectin

ICAM-1, ICAM-3, VCAM-1,

NCAM, ALCAM, VLA-4,

VLA-5, P-selectin, E-selectin

Cytokine receptors FGFR, PDGFR, IL-1R, IFNγR IL-2R

Hematolymphoid CD34* CD4, CD8, CD11b,
markers CD14, CD45
Others MHC class I MHC class II
*Positive in mice but negative in humans. FGFR, Fibroblast growth factor-receptor. PDGFR, Platelet-
derived growth factor-receptor. IL-1R, Interleukin 1-receptor. IL-2 R, Interleukin 2-receptor. IFNγR,
Interferon γ-receptor (unpublished).

However, no specii c markers for MSCs have yet been discovered, thereby making
it dii cult to obtain a purii ed population of MSCs. Very recently, the prospective
isolation of MSCs from whole bone marrow mononuclear cells was attempted
using antibody against SSEA-4 molecule (Gang et al. 2007). MSCs share many
adhesion molecules and cytokines with the niche cells supporting hematopoiesis
(Fig. 1C) . For example, cell adhesion molecules such as ICAM-1, VCAM-1 and
CD44 have been reported to be expressed on mouse and human MSCs. It is known
that cytokines such as IL-6, SCF and M-CSF are produced by MSCs. Indeed, it has
been demonstrated that MSCs have a hematopoiesis-supporting ability. h erefore,
the question arises as to whether the niche cells have dif erentiated from MSCs or
whether MSCs are the cells constituting the niche, and extensive studies to answer
this question are awaited.
h e rolling of MSCs on vascular endothelial cells is an important process
before homing into tissues. Ruster et al. (2006) have demonstrated that MSCs
express P-selectin but a very low level of L-selectin, indicating that MSCs perform
their rolling on the vascular endothelial cells using P-selectin. Zhu et al. (2006)
reported that PDGF stimulation upregulated CD44 expression on rat MSCs,
thereby markedly promoting the migration of the MSCs through hyaluronic acid-
coated membrane. h ey considered such a migration mechanism was critical for
the recruitment of MSCs into wound sites for tissue generation. A more recent
trial indicated that integrin β1 (CD29) was responsible for the migration of MSCs
within the ischemic myocardium in mice, but not integrin α4 (CD49d) or CXC
chemokine receptor 4 (CXCR4) (Ip et al. 2007).