RNCR3: A regulator of diabetes mellitus-related retinal microvascular dysfunction

Biochem Biophys Res Commun. 2017 Jan 22;482(4):777-783. doi: 10.1016/j.bbrc.2016.11.110. Epub 2016 Nov 19.

Abstract

Retinal microvascular abnormality is an important pathological feature of diabetic retinopathy. Herein, we report the role of lncRNA-RNCR3 in diabetes mellitus-induced retinal microvascular abnormalities. We show that RNCR3 is significantly up-regulated upon high glucose stress in vivo and in vitro. RNCR3 knockdown alleviates retinal vascular dysfunction in vivo, as shown by decreased acellular capillaries, decreased vascular leakage, and reduced inflammatory response. RNCR3 knockdown decreases retinal endothelial cell proliferation, and reduces cell migration and tube formation in vitro. RNCR3 regulates endothelial cell function through RNCR3/KLF2/miR-185-5p regulatory network. RNCR3 inhibition may be a treatment option for the prevention of diabetes mellitus-induced retinal microvascular abnormalities.

Keywords: Diabetic retinopathy; Long noncoding RNA; Microvascular abnormalities.

MeSH terms

  • Animals
  • Cell Proliferation
  • Diabetes Complications / metabolism*
  • Diabetic Retinopathy / metabolism*
  • Endothelial Cells / metabolism
  • Gene Silencing
  • Glucose / chemistry
  • Inflammation
  • Male
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Microcirculation
  • Neurons / metabolism
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism
  • Retina / metabolism

Substances

  • MicroRNAs
  • Mirn124 microRNA, mouse
  • RNA, Long Noncoding
  • Glucose