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Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/68213

Title: Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
Authors: Kanda, Atsuhiro Browse this author →KAKEN DB
Dong, Yoko Browse this author
Noda, Kousuke Browse this author →KAKEN DB
Saito, Wataru Browse this author →KAKEN DB
Ishida, Susumu Browse this author →KAKEN DB
Issue Date: 23-Nov-2017
Publisher: Nature Publishing Group
Journal Title: Scientific reports
Volume: 7
Start Page: 16168
Publisher DOI: 10.1038/s41598-017-16499-8
Abstract: Diabetic retinopathy (DR) is an inflammatory and progressive vaso-occlusive disease resulting in angiogenesis. Galectin-1 is a hypoxia-induced angiogenic factor associated with cancer and proliferative DR. Here we reveal a significant upregulation of galectin-1 in eyes of DR patients along with progression of clinical stages beginning from the pre-ischemic, inflammatory stage with diabetic macular edema, but not in eyes with non-diabetic retinal vascular occlusions. As for its regulatory mechanism unrelated to hypoxia but selective to DR, in vitro galectin-1/LGALS1 expression was shown to increase after application to Müller glial cells with interleukin (IL)-1β, which was induced in monocyte-derived macrophages and microglial cells via toll-like receptor (TLR) 4 signaling stimulated by advanced glycation endproducts (AGE). In vivo inhibition of AGE generation with aminoguanidine, macrophage depletion with clodronate liposomes, and antibody-based blockade of Il-1β and Tlr4 attenuated diabetes-induced retinal Lgals1 expression in mice. Fibrovascular tissues from proliferative DR eyes were immunoreactive for AGE, TRL4 and IL-1β in macrophages, and IL-1β receptor-positive glial cells expressed galectin-1. Therefore, diabetes-induced retinal AGE accumulation was suggested to activate IL-1β-related inflammatory cues in macrophages followed by Müller cells, linking to galectin-1 upregulation in human DR with time. Our data highlight AGE-triggered inflammation as the DR-selective inducer of galectin-1.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/68213
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 神田 敦宏

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