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Investigative Ophthalmology & Visual Science, Vol 32, 2689-2695, Copyright © 1991 by Association for Research in Vision and Ophthalmology
ARTICLES AND REPORTS |
Y Uchihori and DG Puro
Department of Ophthalmology, University of Michigan School of Medicine, Ann Arbor.
Glial cell migration and proliferation appear to play a role in many of the proliferative retinopathies. Knowledge concerning the regulation of the migratory and proliferative responses of glial cells to pathophysiologic conditions in the human retina is limited. Here, we report that platelet-derived growth factor (PDGF) has both mitogenic and chemotactic effects on human retinal glial cells in culture. These effects of PDGF support the idea that this growth factor may be one of the molecules influencing glial cell activities in the proliferative retinopathies. Both the mitogenic and chemotactic responses of retinal glial cells to PDGF could be inhibited by the calcium-channel blocker, nifedipine. Although this finding suggests that nifedipine-sensitive calcium channels may help mediate these responses to PDGF, an electrophysiologic effect of PDGF on voltage-gated calcium channels was not detected. Also, the concentration of nifedipine required to inhibit proliferation was higher than the dose needed to block calcium channels. It seems likely that nifedipine inhibits the mitogenic and chemotactic responses of human retinal glial cells to PDGF by affecting cellular processes in addition to calcium channels.
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