조양훈
박재경 이무형 대한피부과학회지 2000년
38권 10호 1315 ~ 1324
Background：Human
growth hormone(hGH) plays a central role in linear
bone growth and body metabolism. Its mitogenic effect
in human tissues is mediated via direct and indirect
actions. As proposed by the "somatomedin hypo
thesis", many circulating GH-mediated effects
are exerted indirectly and systemically via stimulation
of hepatic synthesis of insulin-like growth factor
1(IGF-1). Given additional evidences for the expression
of growth hormone receptor(GH-R) and IGF-1 receptor(IGF-1R)
on many target tissues including keratinocytes,
melanocytes, and fibroblasts, it is now evident
that the GH can act via systemic IGF-1 secreted
by the liver and locally produced IGF-1, as well
as directly through the GH receptor. Objective：The
purpose of this study was to investigate not only
the effect of IGF-1 on the morphologic changes,
proliferation, and melanization of cultured human
melanocytes but also on its signal transduction
pathway through the IGF-1R. Methods：Melanocytes
were exposed to IGF-1 at 10, 25, 50, 75, 100ng/ml
and we examined the changes of cell morphology,
number of cells, [3H]-thymidine incorporation, MTS
assay, and melanization according to the concentrations
and exposure times of IGF-1. Also, the activity
of p44/42 MAPK/ERK according to the various exposure
times of IGF-1(25ng/ml) was examined using the Western
blotting method to find out about the signal transdution
pathway of IGF-1. Results : The results were as
follows： 1. There were no significant morphological
changes of cells between the control and experimental
groups according to the concentrations and exposure
times of IGF-1. 2. The effects on melanocytes according
to the concentrations of IGF-1 5 days after adding
IGF-1 : 1) The number of cells, [3H]-thymidine incorporation,
and MTS assay were significantly higher than those
of control group in all experimental groups(p<0.05).
2) The melanin content showed an insignificant decrease
in all experimental groups. 3) The melanocytes responded
independent of the IGF-1 concentration in the assay
of cell |
