Biomedical Engineering Reference
In-Depth Information
some molecules with fetal hepatoblasts [e.g., α-fetoprotein, delta-like-1 homolog
(Dlk-1)], biliary epithelial cells (cytokeratin-7, -8, -18, -19) and neuroepithelial
cells (chromogranin A and NCAM). h e expression of the neuroepithelial cell
markers suggests that the oval cells are under the control of the central nervous
system and form a neuroendocrine compartment in the liver. Alternatively, it
has been proposed that the oval cells might be derived from bone marrow and
contribute to liver generation, since they also have HSC/HPC-markers such as
h y-1 (CD90), c-kit (CD117) and CD34. h ese observations might indicate that
the oval cells are composed of a heterogeneous population.
Recently, Yovchev
et al.
(2007) identii ed novel oval cell surface markers
in adult rat liver: CD24, CD44, CD133 and epithelial cell adhesion molecule
(EpCAM, CD326). h ey could not, however, detect the expression of some
previously identii ed oval cell markers. In a very recent work, Zhang
et al.
(2008)
isolated two populations from human adult liver: the HpSCs and their progenitors
(hepatoblasts, α-fetoprotein-positive). h e HpSCs proved to have a self-renewal
capacity and to give rise to hepatoblasts by culture and transplantation studies of
immunoselected HpSCs. h e hepatoblasts are transient-amplifying cells and can
dif erentiate into bile epithelial cells and mature hepatocytes. h e HpSCs uniquely
express EpCAM, NCAM and cytokeratin19, but they are only weakly positive for
albumin and are negative for α-fetoprotein.
EpCAM is a transmembrane cell adhesion molecule associated with benign and
malignant cell proliferations. It has been reported that the molecule controls oval
cell migration by modulating the cell-to-cell interactions mediated by cadherin
(Winter
et al.
2003). CD24 is a ligand for P-selectin, and CD44 is suggested to have
a role in oval cell proliferation and migration. h us, great progress has been made
in the identii cation and characterization of the HpSCs themselves, whereas the
niche cells supporting the HpSCs remain to be analyzed.
HAIR FOLLICLE STEM CELLS
Hair follicles repeat the cycle of growth, decline and diapauses throughout life,
and therefore the presence of hair follicle stem cells (HFSCs) has been speculated.
Previously, the HFSCs were thought to reside in the bulbar region of the hair
follicle. Cotsarelis
et al.
(1990), however, proposed that the HFSCs existed in the
bulge area, a contiguous part of the outer root sheath of rodent hair follicles, since
that the bulge is the niche of the HFSCs contributing to both hair follicle cycling
and the repopulation of interfollicular epidermis/sebaceous epithelium. h e
HFSCs generate transient-amplifying cells that migrate to the sebaceous glands,
epidermis and hair bulb and contribute to the formation of the hair follicle.
Recent works have shown that the HFSCs express integrin β1 (CD29), integrin
α6 (CD49f ), keratin 19, CD71, and CD34 to a greater extent than their progenitor
