Document Detail


Retinal pigment epithelium rescues vascular endothelium from retinoic acid-induced apoptosis.
MedLine Citation:
PMID:  17065529     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE: To determine whether retinoids are capable of inducing vascular endothelial cell apoptosis and whether the presence of an intact RPE monolayer can block retinoid-induced vascular endothelial cell death. METHODS: Confluent fetal bovine aortic endothelial (FBAE) cells were incubated with various concentrations of all-trans or 9-cis retinoic acid (an analogue of 11-cis retinoic acid). Apoptosis rates were determined at 24 hours, and the effect of inhibition of protein synthesis and activation of protein kinase C on apoptosis was investigated by supplying culture medium with 0.1 mg/mL cycloheximide and 10 nM phorbol myristate acetate. To investigate the impact of RPE on retinoid-induced apoptosis, confluent FBAE cells were cultured with a confluent layer of RPE in inserts where retinoids were added to the upper compartment. A confluent bovine corneal endothelium monolayer was used as the control. The permeabilities of the RPE and bovine corneal endothelium monolayers to fluorescein (20 microg/mL) and 9-cis retinoic acid (3 x 10(-4) M) were also determined. RESULTS: 9-cis Retinoic acid induced higher rates of apoptosis in FBAE cells than did all-trans retinoic acid and the control (P = 0.004). This effect was dose-dependent, with an ED(50) of 1.4 microM (r = 0.99, P = 0.004). Cycloheximide did not inhibit 9-cis retinoic acid-induced apoptosis, but phorbol myristate acetate significantly decreased the apoptosis rate (P = 0.005). The presence of a confluent RPE monolayer reduced the 9-cis retinoic acid-induced apoptosis rate (P = 0.002), but the presence of a bovine corneal endothelial monolayer did not (P > 0.05). Both cell types established a similar diffusion barrier against fluorescein and 9-cis retinoic acid. CONCLUSIONS: 9-cis Retinoic acid is an important mediator of vascular endothelial apoptosis. A confluent monolayer of RPE can prevent endothelial cell apoptosis, and this effect is not due simply to establishment of a diffusion barrier by the RPE.
Authors:
Tongalp H Tezel; Lijun Geng; Henry J Kaplan; Lucian V Del Priore
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Investigative ophthalmology & visual science     Volume:  47     ISSN:  0146-0404     ISO Abbreviation:  Invest. Ophthalmol. Vis. Sci.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-26     Completed Date:  2006-12-08     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7703701     Medline TA:  Invest Ophthalmol Vis Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5075-87     Citation Subset:  IM    
Affiliation:
Department of Ophthalmology and Visual Sciences, Kentucky Lions Eye Center, University of Louisville School of Medicine, 301 E. Muhammad Ali Boulevard, Louisville, KY 40202, USA. tongalp.tezel@louisville.edu
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Animals
Aorta, Thoracic / cytology
Apoptosis / drug effects*
Cattle
Cell Culture Techniques
Cell Survival / physiology
Coculture Techniques
Cycloheximide / pharmacology
Dose-Response Relationship, Drug
Endothelium, Vascular / cytology*,  drug effects,  metabolism
Flow Cytometry
Humans
Microscopy, Fluorescence
Pigment Epithelium of Eye / physiology*
Protein Kinase C / metabolism
Tetradecanoylphorbol Acetate / pharmacology
Tretinoin / pharmacology*
Grant Support
ID/Acronym/Agency:
EY 016120/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
16561-29-8/Tetradecanoylphorbol Acetate; 302-79-4/Tretinoin; 5300-03-8/alitretinoin; 66-81-9/Cycloheximide; EC 2.7.11.13/Protein Kinase C

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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