IOVS Infection and Immunity
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

(Investigative Ophthalmology and Visual Science. 2006;47:4547-4552.)
© 2006 by The Association for Research in Vision and Ophthalmology, Inc.
DOI:  10.1167/iovs.05-1432
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (2)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Muranaka, K.
Right arrow Articles by Araie, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Muranaka, K.
Right arrow Articles by Araie, M.

Effects of Peroxisome Proliferator-Activated Receptor {gamma} and Its Ligand on Blood–Retinal Barrier in a Streptozotocin-Induced Diabetic Model

Kimimasa Muranaka,1 Yasuo Yanagi,1 Yasuhiro Tamaki,1 Tomohiko Usui,1 Naoto Kubota,2 Aya Iriyama,1 Yasuo Terauchi,2 Takashi Kadowaki,3 and Makoto Araie1

1From the Department of Ophthalmology, University of Tokyo School of Medicine, Tokyo, Japan; the 2Department of Endocrinology and Metabolism, Yokohama City University Graduate School of Medicine, Yokohama, Japan; and the 3Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.

PURPOSE. To clarify whether endogenous peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) and its ligand, rosiglitazone, affect retinal leukostasis and the associated vascular leakage using an experimental diabetic model.

METHODS. Diabetes was induced in heterozygous PPAR{gamma}+/– mice and Brown Norway rats with an intraperitoneal streptozotocin (STZ) injection. Retinal leukostasis and leakage, quantified by concanavalin A (Con A) lectin perfusion labeling combined with a fluorophotometric dextran leakage assay, were investigated at 120 days in diabetic PPAR{gamma}+/– and wild-type mice and at 21 days in diabetic rats receiving rosiglitazone or the vehicle. The retinal protein expression levels of vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF)-{alpha}, and the intercellular adhesion molecule (ICAM)-1 were investigated by means of the ELISA assay.

RESULTS. In the diabetic PPAR{gamma}+/– mice, retinal leukostasis and leakage were greater than in the diabetic wild-type mice. In addition retinal leukostasis and leakage were suppressed by treatment with rosiglitazone in experimental diabetic rats. ELISA analysis revealed that the upregulated ICAM-1 expression in the diabetic rat retina was reduced by rosiglitazone treatment.

CONCLUSIONS. An endogenous pathway involving PPAR{gamma} provides protection against retinal leukostasis and retinal leakage in diabetes and treatment with PPAR{gamma} specific ligands inhibits retinal leukostasis and retinal leakage in diabetic rats.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the Association for Research in Vision and Ophthalmology