Experimental proliferative vitreoretinopathy (PVR) was induced in the rabbi
t eye by injecting mitotically active Muller cells into the vitreal chamber
. Two weeks after the initiation of PVR, the retina and the epiretinal memb
rane that formed were examined to ascertain the antigenic expression of Mul
ler cells in the retina and in the epiretinal membrane. Examination of vari
ous regions of the retina from the experimental PVR eye demonstrated that v
imentin, glial fibrillary acidic protein (GFAP), cellular retinaldehyde bin
ding protein (CRALBP), and beta-amyloid precursor protein (beta-APP), which
were present in the Muller cells of the retina from the control eye, incre
ased their expression, while the antigenicity of glutamine synthetase (GS),
did not change; these proteins were also present in the cells contained wi
thin the experimentally induced epiretinal membrane. Alpha smooth muscle ac
tin (alpha-SMA), a cytoskeletal protein that is associated with migration a
nd tractional forces in many cell types, was not only present in the cells
embedded within the epiretinal membrane, but was also present in the Muller
cells underlying the epiretinal membrane. However, Muller cells that were
in the inferior portion of the retina, where epiretinal membrane pathology
was absent, did not express alpha-SMA. Although this protein is not normall
y found in Muller cells, they do express it de novo when they are maintaine
d in culture. This suggests that a localized mechanism associated with epir
etinal membrane formation induces the expression of alpha-SMA in Muller cel
ls while the increased expression of GFAP, beta-APP, vimentin, and CRALBP a
re probably regulated via a more general mechanism. (C) 1999 Academic Press
.