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

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...

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Autores principales:	Atsuhiro Kanda, Yoko Dong, Kousuke Noda, Wataru Saito, Susumu Ishida
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/129dedc23cca450e945e7b70fb0c324f
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spelling	oai:doaj.org-article:129dedc23cca450e945e7b70fb0c324f2021-12-02T15:06:07ZAdvanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy10.1038/s41598-017-16499-82045-2322https://doaj.org/article/129dedc23cca450e945e7b70fb0c324f2017-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-16499-8https://doaj.org/toc/2045-2322Abstract 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.Atsuhiro KandaYoko DongKousuke NodaWataru SaitoSusumu IshidaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-15 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Atsuhiro Kanda Yoko Dong Kousuke Noda Wataru Saito Susumu Ishida Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
description	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.
format	article
author	Atsuhiro Kanda Yoko Dong Kousuke Noda Wataru Saito Susumu Ishida
author_facet	Atsuhiro Kanda Yoko Dong Kousuke Noda Wataru Saito Susumu Ishida
author_sort	Atsuhiro Kanda
title	Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
title_short	Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
title_full	Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
title_fullStr	Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
title_full_unstemmed	Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
title_sort	advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/129dedc23cca450e945e7b70fb0c324f
work_keys_str_mv	AT atsuhirokanda advancedglycationendproductslinkinflammatorycuestoupregulationofgalectin1indiabeticretinopathy AT yokodong advancedglycationendproductslinkinflammatorycuestoupregulationofgalectin1indiabeticretinopathy AT kousukenoda advancedglycationendproductslinkinflammatorycuestoupregulationofgalectin1indiabeticretinopathy AT watarusaito advancedglycationendproductslinkinflammatorycuestoupregulationofgalectin1indiabeticretinopathy AT susumuishida advancedglycationendproductslinkinflammatorycuestoupregulationofgalectin1indiabeticretinopathy
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Advanced glycation endproducts link inflammatory cues to upregulation of galectin-1 in diabetic retinopathy

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