Biomedical Engineering Reference
In-Depth Information
Fig. 1
Immunohistochemical expression of β-catenin, cadherins and a marker of melanosomes,
the hair matrical tumor called melanocytic matricoma. Expression of β-catenin (A), E-cadherin
(B), P-cadherin (C) and HMB45, a marker of melanosomes (D) in a melanocytic matricoma.
Nuclear β-catenin (arrow) is seen in the basal cells but not in the more dif erentiated keratinized
cells (k). E- and P-cadherin show cell membrane distribution typical of their cell-cell adhesion
function. h e expression of HMB45 (arrows) highlights the presence of numerous dendritic cells
that characterize this tumor. Scale bar = 200 μm.
Matrical Nail Tumors
In contrast to the signals mediating the development of hairs and teeth, the signals
regulating the development of the nail are still poorly understood, although it is
known that the interaction between epithelium and mesenchymal tissue plays a
signii cant role in nail development (Bergmann
et al.
2006). Furthermore, there are
dif erences between the mechanisms of hair development and nail development.
Hair growth is a cyclic process that alternates between growth and rest phases.
In contrast, the nail grows continuously. h e growth rate of nails is the result
of cell proliferation of the matrix and mechanisms of terminal dif erentiation.
h e growth and development of hairs is known to depend on the presence of
activated β-catenin in the matrix cells (Gat
et al.
1998). In contrast, growth of
nails appears to depend on the activation of signals in dif erent portions of the
nail. On one hand, nail growth and increased cell proliferation can be triggered
by activation of Notch1 in post-mitotic keratinized cells. h is results in activation
of Wnt signaling but no β-catenin in nail matrix cells (Lin and Kopan 2003).
