Embryonic chick retinal pigment epithelial (RPE)
cells can undergo transdifferentiation upon appropriate
stimulation. For example, basic fibroblast growth factor
(bFGF) induces intact RPE tissue younger than embryonic
day 4.5 (E4.5) to transdifferentiate into a neural retina.
NeuroD, a gene encoding a basic helix-loop–helix
transcription factor, triggers de novo production
of cells that resemble young photoreceptor cells morphologically
and express general neuron markers (HNK-1/N-CAM and MAP2)
and a photoreceptor-specific marker (visinin)
from cell cultures of dissociated E6 RPE (Yan & Wang,
1998). The present study examined whether bFGF will lead
to the same transdifferentiation phenomenon as neuroD
when applied to dissociated, cultured E6 RPE cells, and
whether interplay exists between the two factors under
the culture conditions. Dissociated E6 RPE cells were cultured
in the presence or absence of bFGF, and with or without
the addition of retrovirus expressing neuroD.
Gene expression was analyzed with immunocytochemistry and
in situ hybridization. Unlike neuroD,
bFGF did not induce the expression of visinin,
or HNK-1/N-CAM and MAP2. However, bFGF elicited the expression
of RA4 immunogenicity; yet, many of these RA4-positive
cells lacked a neuronal morphology. Addition of bFGF to
neuroD-expressing cultures did not alter the number
of visinin-expressing cells; misexpression of
neuroD in bFGF-treated cultures did not change
the number of RA4-positive cells, suggesting the absence
of interference or synergistic interaction between the
two factors. Our data indicated that bFGF and neuroD
induced the expression of different genes in cultured RPE
cells.
Basic fibroblast growth factor inhibits type I collagen gene expression in osteoblastic MC3T3-E1 cells.
