miR-106b suppresses pathological retinal angiogenesis

Cathérine Ménard, Ariel M. Wilson, Agnieszka Dejda, Khalil Miloudi, François Binet, Sergio Crespo-Garcia, Célia Parinot, Frédérique Pilon, Rachel Juneau, Elisabeth MMA Andriessen, Gaëlle Mawambo, John Paul SanGiovanni, Vincent De Guire, Przemyslaw Sapieha

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


MicroRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. We recently demonstrated that levels of miR-106b were significantly decreased in the vitreous and plasma of patients with neovascular age-related macular degeneration (AMD). Here we show that expression of the miR-106b-25 cluster is negatively regulated by the unfolded protein response pathway of protein kinase RNA-like ER kinase (PERK) in a mouse model of neovascular AMD. A reduction in levels of miR-106b triggers vascular growth both in vivo and in vitro by inducing production of pro-angiogenic factors. We demonstrate that therapeutic delivery of miR-106b to the retina with lentiviral vectors protects against aberrant retinal angiogenesis in two distinct mouse models of pathological retinal neovascularization. Results from this study suggest that miRNAs such as miR-106b have the potential to be used as multitarget therapeutics for conditions characterized by pathological retinal angiogenesis.

Original languageEnglish (US)
Pages (from-to)24836-24852
Number of pages17
Issue number24
StatePublished - Dec 31 2020


  • PERK
  • age related macular degeneration
  • angiogenesis
  • choroidal neovascularization
  • miR-106b

ASJC Scopus subject areas

  • Aging
  • Cell Biology


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