Journal
CYTOKINE
Volume 104, Issue -, Pages 147-150Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2017.10.009
Keywords
BRAF-activated non-coding RNA (BANCR); Long non-coding RNA (lncRNA); Interferon-gamma; JAK-STAT1 signaling; Retinal pigment epithelium; Age-related macular degeneration
Funding
- National Eye Institute, NIH
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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-gamma, IL-1 beta and TNF-alpha 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-gamma. BANCR expression induced by IFN-gamma 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-gamma could upregulate the expression of BANCR by activating JAK-STAT1 signaling pathway.
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