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Atsuhiro Kanda, Ikuyo Hirose, Kousuke Noda, Susumu Ishida; Transcriptional suppression of galectin-1/LGALS1 by glucocorticoids in Müller glial cells and diabetic retinopathy. Invest. Ophthalmol. Vis. Sci. 2019;60(9):2650.
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Galectin-1/LGALS1 is a hypoxia-induced angiogenic factor associated with cancer and diabetic retinopathy (DR). Recently, we elucidated a hypoxia-independent inflammatory pathway to produce galectin-1 in retinal Müller glial cells stimulated by interleukin (IL)-1β. The aim of this study was to investigate the regulatory mechanism of galectin-1/LGALS1 gene expression in IL-1β signaling.
Immunoblot and real-time PCR analyses were performed to measure protein and mRNA expression levels in human Müller glial cells and the retina of mice with streptozotocin-induced diabetes. Human surgical samples from proliferative DR eyes were examined by immunofluorescence.
Glucocorticoid drugs dexamethasone (Dex) and triamcinolone acetonide (TA) significantly (p < 0.05 for all) attenuated IL-1β-mediatedglial and diabetes-induced retinal expression of galectin-1/LGALS1 (fold change with IL-1β = 2.0, plus Dex= 1.41, plus TA = 1.41; fold change with diabetes= 5.21, plus Dex= 2.57, plus TA = 2.10) together with reduced phosphorylation of the serine/threonine kinase AKT (also known as protein kinase B) and extracellular signal-regulated kinases (ERK)1/2. Supporting these in vitro and in vivo findings, immunofluorescence showed co-localization of galectin-1 with the glucocorticoid receptorin glial cells in the fibrovascular tissue surgically extracted from eyes of patients with proliferative DR.
Our present findings demonstrated the inhibitory action of glucocorticoids on IL-1β-stimulated and diabetes-induced galectin-1/LGALS1 gene expression, which is modulated by AKT and ERK1/2.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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