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

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

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.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Adult
  • Cell Line
  • Epithelial Cells / metabolism*
  • Gene Expression Regulation*
  • Humans
  • Inflammation Mediators / metabolism*
  • Interferon-gamma / metabolism*
  • RNA, Long Noncoding / genetics*
  • RNA, Long Noncoding / metabolism
  • Retinal Pigment Epithelium / metabolism*

Substances

  • BANCR long non-coding RNA, human
  • Inflammation Mediators
  • RNA, Long Noncoding
  • Interferon-gamma