Epinephrine, but not dexamethasone, induces apoptosis in retinal pigment epithelium cells in vitro: possible implications an the pathogenesis of central serous chorioretinopathy

Citation
Sab. Sibayan et al., Epinephrine, but not dexamethasone, induces apoptosis in retinal pigment epithelium cells in vitro: possible implications an the pathogenesis of central serous chorioretinopathy, GR ARCH CL, 238(6), 2000, pp. 515-519
Citations number
35
Categorie Soggetti
Optalmology
Journal title
GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY
ISSN journal
0721832X → ACNP
Volume
238
Issue
6
Year of publication
2000
Pages
515 - 519
Database
ISI
SICI code
0721-832X(200006)238:6<515:EBNDIA>2.0.ZU;2-O
Abstract
Background: The pathogenesis of central serous chorioretinopathy is poorly understood. It is believed to be due to dysfunction of the retinal pigment epithelium and/or choroid and has been associated with elevated levels of e pinephrine and administration of corticosteroids. Epinephrine and corticost eroids have previously been shown to induce apoptosis (programmed cell deat h) in various types of cells. The objective of this study was to investigat e whether these agents can induce apoptosis in cultured retinal pigment epi thelium cells. This may help elucidate the pathogenesis of central serous c horioretinopathy. Methods: Third-passage porcine retinal pigment epithelium cells were grown to confluence and incubated for 1-7 days in culture medium containing epine phrine (10(2)-10(9) pg/ml) or a corticosteroid, dexamethasone (4-4x10(4) ng /ml). The cultures were evaluated for apoptosis by phase-contrast microscop y and in situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. Results: Epinephrine (7x10(7)-10(9) pg/ml) induced apoptosis in a dose- and time-dependent manner. Exposure to lower concentrations of epine phrine(10(2)-6x10(7) pg/ml) and all tested levels of dexamethasone did not result in apoptosis. Conclusion: Retinal pigment epithelium cells may undergo apoptosis followin g exposure to elevated levels of epinephrine. These findings suggest a poss ible pathophysiologic mechanism for the development of central serous chori oretinopathy.