Abstract
Purpose :
In recent years, Müller glial cell (MGC) derived Galectin (Gal) -1 and -3 have been found to be key regulators of various cellular processes within the retina. This study aims to investigate the potential roles of Gal-1 and -3 following inflammatory stimuli.
Methods :
Experiments were conducted using the Moorfields Institute of Ophthalmology Müller 1 (MIO-M1) cell line. Hexosaminidase assay was used to quantify the rate of proliferation and scratch assay was used to assess the rate of migration. Quantitative RT-PCR and RNA-Seq were used to investigate mRNA expression, whilst western blot and immunohistochemical staining were used to investigate protein expression levels.
Results :
MIO-M1 cells treatment with IL-1 resulted in significantly upregulated production of Gal-1 (p<.01) and ST3GAL1 (p<.01), whereas treatment with TGF-β significantly reduced the production of Gal-3 (p<.001) but had no significant effect on ST6GAL1 (p>.05). Inhibition of Gal-3 via siRNA decreased the rate of cell proliferation (p<.001) and contraction (p<0.01). TGF-β2 treatment increased the rate of migration (p<.01), but this effect was nullified following Gal-3 siRNA inhibition. Gal-3 was found to increase TGF-β induced SMAD phosphorylation and β-catenin activation, whilst Gal-1 was found to increase TNF-α induced STAT3 phosphorylation.
Conclusions :
influenced by the presence of cytokines such as IL-1 and TGF-β. Furthermore, Gal-1 and -3 also appeared to significant influence important cellular processes via intracellular pathways. As such, manipulation of Gal-1 and -3 expression may have therapeutic potential for retinal diseases.
This abstract was presented at the 2023 ARVO Annual Meeting, held in New Orleans, LA, April 23-27, 2023.