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Swaminathan Sethu, Archana Padmanabhan Nair Nair, Praveen Machiraju, Murugeswari Ponnalagu, Anuprita Ghosh, Sushma Tejwani, Arkasubhra Ghosh; Association of interferon beta and erythropoietin levels with disease severity in glaucoma. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3730. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Glaucoma is one of the major cause of irreversible blindness worldwide. Current strategies in the management of glaucoma are directed against reducing IOP, but progression of neurodegeneration continues despite managing IOP in some patients. This suggests the need to explore molecular factors that may contribute to disease progression. Interferon beta (IFNb) has been used quite effectively in the management of neurodegenerative conditions, hence its endogenous status in glaucoma is worthy of investigation.
Aqueous humour (AH) and iris were obtained during surgical intervention in patients with glaucoma (n=20) without deviating from standard of care and after obtaining their written informed consent and approval by the institutional ethics committee. The subjects were categorized based on severity of glaucoma by visual field index scores (severe, < 40) as severe (n=11) and nonsevere (n=9). IFNb levels in AH was measured by ELISA. mRNA levels of IFNB, interferon inducible Myxovirus resistance protein 1 – MxA, Erythropoietin – EPO and Lipocalin 2 – LCN2 in iris and primary retinal pigment epithelial cells – PRPE from cadaveric controls (n=5) were quantified by qPCR. Furthermore, the expression of these genes was also measured in ARPE19 cells treated with rhIFNb for 24 hrs. Statistical analysis was done using Graphpad prism.
Levels of IFNb in AH was significantly lower in patients with severe (193±34pg/ug) compared to nonsevere (424±26pg/ug) stage of glaucoma. Similary, IFNb expression in the iris was significantly lower by -8.3 fold in severe (0.05±0.02) compared to nonsevere (0.4±0.1) form. In addition, the expression of LCN2 (marker of nerve injury) was significantly higher (8.1 fold) and the expression of EPO (a neuroprotective factor) was -3.7 fold lower in the iris of patients with severe compared to nonsevere stage of glaucoma. A positive correlation (r=0.695, p≤0.05) was observed between the basal expression of MxA and EPO in PRPE. Furthermore, we observed an increase in the expression of MxA and EPO in ARPE19 cells treated with rhIFNb.
Lower levels of IFNb and EPO in severe glaucoma suggests their plausible role in neuroprotection and increased levels of LCN2 suggests its potential as a biomarker for nerve injury status in glaucoma. IFNb induction of neuroprotective factors such as EPO by RPE can be beneficial in neurodegenerative conditions.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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