| Literature DB >> 29054724 |
R Krishnan Kutty1, William Samuel2, Todd Duncan2, Olga Postnikova2, Cynthia Jaworski2, Chandrasekharam N Nagineni3, T Michael Redmond2.
Abstract
The inflammatory response may contribute to retinal pigment epithelial (RPE) dysfunction associated with the pathogenesis of age-related macular degeneration (AMD). We investigated whether the inflammatory response affects the expression of long coding RNAs (lncRNAs) in human RPE-derived ARPE-19 cells. This class of regulatory RNA molecules recently came to prominence due to their involvement in many pathophysiological processes. A proinflammatory cytokine mixture consisting of IFN-γ, IL-1β and TNF-α altered the expression several lncRNAs including BANCR in these cells. The cytokine responsible for increasing BANCR expression in ARPE-19 cells was found to be IFN-γ. BANCR expression induced by IFN-γ was suppressed when STAT1 phosphorylation was blocked by JAK inhibitor 1. Thus, proinflammatory cytokines could modulate the expression of lncRNAs in RPE cells and IFN-γ could upregulate the expression of BANCR by activating JAK-STAT1 signaling pathway. Published by Elsevier Ltd.Entities:
Keywords: Age-related macular degeneration; BRAF-activated non-coding RNA (BANCR); Interferon-γ; JAK-STAT1 signaling; Long non-coding RNA (lncRNA); Retinal pigment epithelium
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Year: 2017 PMID: 29054724 PMCID: PMC5847440 DOI: 10.1016/j.cyto.2017.10.009
Source DB: PubMed Journal: Cytokine ISSN: 1043-4666 Impact factor: 3.861