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Cytokine. 2018 Apr;104:147-150. doi: 10.1016/j.cyto.2017.10.009. Epub 2017 Oct 18.

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

Author information

1
Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: kuttyk@nei.nih.gov.
2
Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, United States.
3
Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States.

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.

KEYWORDS:

Age-related macular degeneration; BRAF-activated non-coding RNA (BANCR); Interferon-γ; JAK-STAT1 signaling; Long non-coding RNA (lncRNA); Retinal pigment epithelium

PMID:
29054724
PMCID:
PMC5847440
[Available on 2019-04-01]
DOI:
10.1016/j.cyto.2017.10.009

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