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P33
C-MYC, MAX AND BIN1 EXPRESSION IN HUMAN ANAGEN HAIR FOLLICLES.
Barajon I., Donetti E., Rumio C., Imberti A., Castano P.;
Institute of Human Anatomy, University of Milan, Via Mangiagalli
31, 20133 Milan, Italy.
Recently, we have shown the presence of c-Myc immunoreactivity
in three distinct zones of the IRS, corresponding to the level
where terminal differentiation takes place in Henles,
cuticles and Huxleys layers. On this background
we have decided to extend our investigations to two others
regulatory molecules participating to the so-called Myc
network: Max and Bin1.
Human scalp microislets were processed for immunofluorescence
and immunohistochemical detection of c-Myc, Max and Bin1 and
Western blot analysis was performed for the latter. The subcellular
localization of the immunoreactivity was mostly cytoplasmic.
Max immunostaining was present in all the three layers of
the IRS, starting where they become distinguishable at the
level of the bulb. Bin1 immunostaining could be detected in
Huxleys layer and in the cuticle starting from the keratogenic
zone. Both for Max and Bin1, the labeling stopped in each
layer at the level of the corresponding c-Myc positive ring
where there was a rather complete overlapping among the immunoreactivies.
Clear-cut Bin1 immunostaining was also present in the companion
layer of the ORS up to the infundibular region. A correlation
between the immunostaining for Max and Bin1 and changes in
the morphological features of cells could be clearly observed
at the level of the c-Myc rings, consisting in a rather abrupt
disappearance of putative trichoyalin granules, nuclear picnosis
and changes in the appearance of the cytoplasm. The results
of the present study indicate that behind the biochemical
events leading to terminal differentiation of hair follicle
keratinocytes there is complex balance of Myc-interacting
molecules suggesting also that this small organ could provide
a useful model to investigate the expression of genes usually
involved in cell transformation, tumorigenesis and tumor suppression.
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