Rabbit retinal Müller cells undergo antigenic changes in response to experimentally induced proliferative vitreoretinopathy.

Experimental proliferative vitreoretinopathy (PVR) was induced in the rabbit eye by injecting mitotically active Müller cells into the vitreal chamber. Two weeks after the initiation of PVR, the retina and the epiretinal membrane that formed were examined to ascertain the antigenic expression of Müller cells in the retina and in the epiretinal membrane. Examination of various regions of the retina from the experimental PVR eye demonstrated that vimentin, glial fibrillary acidic protein (GFAP), cellular retinaldehyde binding protein (CRALBP), and beta-amyloid precursor protein (beta-APP), which were present in the Müller cells of the retina from the control eye, increased their expression, while the antigenicity of glutamine synthetase (GS), did not change; these proteins were also present in the cells contained within the experimentally induced epiretinal membrane. Alpha smooth muscle actin (alpha-SMA), a cytoskeletal protein that is associated with migration and tractional forces in many cell types, was not only present in the cells embedded within the epiretinal membrane, but was also present in the Müller cells underlying the epiretinal membrane. However, Müller 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 normally found in Müller cells, they do express it de novo when they are maintained in culture. This suggests that a localized mechanism associated with epiretinal membrane formation induces the expression of alpha-SMA in Müller cells while the increased expression of GFAP, beta-APP, vimentin, and CRALBP are probably regulated via a more general mechanism.