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. 2020 Feb;98(1):e1-e12.
doi: 10.1111/aos.14191. Epub 2019 Jul 18.

Galectin-1 studies in proliferative diabetic retinopathy

Ahmed M Abu El-Asrar  1   2 , Ajmal Ahmad  1 , Eef Allegaert  3 , Mohammad Mairaj Siddiquei  1 , Kaiser Alam  1 , Priscilla W Gikandi  1 , Gert De Hertogh  3 , Ghislain Opdenakker  4
Affiliations
Free article

Galectin-1 studies in proliferative diabetic retinopathy

Ahmed M Abu El-Asrar et al. Acta Ophthalmol. 2020 Feb.
Free article

Abstract

Purpose: Galectin-1 regulates endothelial cell function and promotes angiogenesis. We investigated the hypothesis that galectin-1 may be involved in the pathogenesis of proliferative diabetic retinopathy (PDR).

Methods: Vitreous samples from 36 PDR and 20 nondiabetic patients, epiretinal fibrovascular membranes from 13 patients with PDR, rat retinas and human retinal Müller glial cells were studied by enzyme-linked immunosorbent assay (ELISA), immunohistochemistry and Western blot analysis. In vitro angiogenesis assays were performed and the adherence of leukocytes to galectin-1-stimulated human retinal microvascular endothelial cells (HRMECs) was assessed.

Results: The ELISA analysis revealed that galectin-1 and vascular endothelial growth factor (VEGF) levels were significantly higher in vitreous samples from PDR patients than in those from nondiabetics (p < 0.001 for both comparisons). A significant positive correlation was found between the levels of galectin-1 and VEGF (r = 0.354; p = 0.022). In epiretinal membranes, immunohistochemical analysis showed that galectin-1 was expressed in vascular endothelial cells expressing CD31, myofibroblasts expressing α-smooth muscle actin and leukocytes expressing CD45. The galectin-1 receptor neuropilin-1 was expressed on vascular endothelial cells. CD31 staining was used as a marker to assess microvessel density (MVD). Significant positive correlation was detected between MVD in epiretinal membranes and the number of blood vessels expressing galectin-1 (r = 0.848; p < 0.001). Western blot analysis demonstrated significant increase of galectin-1 protein in rat retinas after induction of diabetes. ELISA analysis revealed that hydrogen peroxide and cobalt chloride (CoCl2 ) induced upregulation of galectin-1 in Müller cells. Treatment with galectin-1 induced upregulation of VEGF in Müller cells and increased leukocyte adhesion to HRMECs. The galectin-1 inhibitor OTX008 attenuated VEGF-induced HRMECs migration and CoCl2 -induced upregulation of NF-κB, galectin-1 and VEGF in Müller cells.

Conclusions: These results suggest that galectin-1is involved in the pathogenesis of PDR.

Keywords: Müller cells; angiogenesis; galectin-1; neuropilin-1; proliferative diabetic retinopathy.

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References

    1. Abu El-Asrar AM, Struyf S, Van Damme J & Geboes K (2008): Circulating fibrocytes contribute to the myofibroblast population in proliferative vitreoretinopathy epiretinal membranes. Br J Ophthalmol 92: 699-704.
    1. Abu El-Asrar AM, Missotten L & Geboes K (2011): Expression of myofibroblast activation molecules in proliferative vitreoretinopathy epiretinal membranes. Acta Ophthalmol 89: e115-e121.
    1. Abu El-Asrar AM, Mohammad G, Nawaz MI, Siddique MM, Van den Eynde K, Mousa A, De Hertogh G & Opdenakker G (2013a): Relationship between vitreous levels of matrix metalloproteinases and vascular endothelial growth factor in proliferative diabetic retinopathy. PLoS ONE 8: e85857.
    1. Abu El-Asrar AM, Nawaz MI, Kangave D, Siddique MM & Geboes K (2013b): Angiogenic and vasculogenic factors in the vitreous from patients with proliferative diabetic retinopathy. J Diabetes Res 2013:539-658.
    1. Abu El-Asrar AM, Nawaz MI, De Hertogh G et al. (2014): S100A4 is upregulated in proliferative diabetic retinopathy and correlates with markers of angiogenesis and fibrogenesis. Mol Vis 20: 1209-1224.

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