Proinflammatory cytokine interferon-γ increases the expression of BANCR, a long non-coding RNA, in retinal pigment...

Area of Science:

• Ophthalmology
• Molecular Biology
• Immunology

Background:

• Age-related macular degeneration (AMD) pathogenesis involves retinal pigment epithelial (RPE) dysfunction.
• The inflammatory response is implicated in RPE dysfunction.
• Long non-coding RNAs (lncRNAs) are regulatory molecules involved in pathophysiological processes.

Purpose of the Study:

• To investigate the effect of inflammatory response on lncRNA expression in human RPE-derived ARPE-19 cells.
• To identify specific cytokines and signaling pathways involved in modulating lncRNA expression in RPE cells.

Main Methods:

• ARPE-19 cells were treated with a proinflammatory cytokine mixture (IFN-γ, IL-1β, TNF-α).
• Expression levels of lncRNAs, including BANCR, were analyzed.
• The role of IFN-γ and the JAK-STAT1 pathway in BANCR regulation was assessed using JAK inhibitor 1.

Main Results:

• A mixture of proinflammatory cytokines altered the expression of several lncRNAs in ARPE-19 cells.
• IFN-γ was identified as the specific cytokine that increased BANCR expression.
• IFN-γ-induced BANCR upregulation was suppressed by blocking STAT1 phosphorylation with a JAK inhibitor.

Conclusions:

• Proinflammatory cytokines can modulate lncRNA expression in RPE cells.
• IFN-γ upregulates BANCR expression in RPE cells through the activation of the JAK-STAT1 signaling pathway.
• These findings provide insights into the molecular mechanisms underlying RPE dysfunction in AMD.