Abstract
Purpose :
Galectin-1, a newly recognized hypoxia-induced angiogenic factor, increased in the vitreous of eyes with proliferative diabetic retinopathy (PDR) independently of vascular endothelial growth factor (VEGF)-A (Kanda A, et al., 2015 Sci Rep.). Recently, we reported that advanced glycation end products (AGEs)-induced interleukin (IL)-1β caused the retinal elevation of galectin-1 (Kanda A, et al., 2017 Sci Rep.). In this study, we explored correlations between protein levels of galectin-1 and potentially related molecules in plasma of patients with PDR.
Methods :
Plasma samples were obtained from 40 patients, including 20 non-diabetic cases with idiopathic macular diseases (aged 63.4 ± 1.0 y/o), and 20 cases with PDR (aged 62.4 ± 1.9 y/o). Plasma levels of galectin-1, and inflammation-associated and/or hypoxia-induced molecules AGEs IL-1β, IL-6, C-reactive protein (CRP), erythropoietin, lactate dehydrogenase (LDH) and VEGF-A were determined by using a multiplex bead analysis system and enzyme-linked immunosorbent assay.
Results :
As compared with those in non-diabetic patients, plasma levels of galectin-1, AGEs and IL-1β significantly increased in patients with PDR (p < 0.01), but IL-6, CRP, erythropoietin, LDH, and VEGF-A levels did not (p > 0.05). Increased plasma galectin-1 levels were positively correlated with AGEs and IL-1β levels in patients with PDR (p < 0.01), but not in non-diabetic controls (p > 0.05).
Conclusions :
In consistent with our recent report, the current data suggest that AGEs upregulate plasma galectin-1 via IL-1β, although the cellular components involved in the eye are different. Increased plasma galectin-1 may result from AGE-triggered inflammatory stimuli rather than hypoxic induction.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.