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Publication Detail
Mir-96 and miR-183 differentially regulate neonatal and adult post-infarct neovascularisation.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Castellan RF, Vitiello M, Vidmar M, Johnstone S, Iacobazzi D, Mellis D, Cathcart B, Thomson AJ, Ruhrberg C, Caputo M, Newby DE, Gray GA, Baker AH, Caporali A, Meloni M
  • Publication date:
    16/06/2020
  • Journal:
    JCI Insight
  • Status:
    Published
  • Country:
    United States
  • PII:
    134888
  • Language:
    eng
  • Keywords:
    Angiogenesis, Cardiovascular disease, Vascular Biology
Abstract
Following myocardial infarction (MI), the adult heart has minimal regenerative potential. Conversely, the neonatal heart can undergo extensive regeneration, and neovascularisation capacity was hypothesised to contribute to this difference. Here, we demonstrate the higher angiogenic potential of neonatal compared to adult mouse cardiac endothelial cells (MCECs) in vitro and use this difference to identify candidate microRNAs (miRs) regulating cardiac angiogenesis after MI. MiR expression profiling revealed miR-96 and miR-183 upregulation in adult compared to neonatal MCECs. Their overexpression decreased the angiogenic potential of neonatal MCECs in vitro and prevented scar resolution and neovascularisation in neonatal mice after MI. Inversely, their inhibition improved the angiogenic potential of adult MCECs, and miR-96/miR-183 knock-out mice had increased peri-infarct neovascularisation. In silico analyses identified anillin (ANLN) as a direct target of miR-96 and miR-183. In agreement, Anln expression declined following their overexpression and increased after their inhibition in vitro. Moreover, ANLN expression inversely correlated with miR-96 expression and age in cardiac ECs of cardiovascular patients. In vivo, ANLN-positive vessels were enriched in the peri-infarct area of miR-96/miR-183 knock-out mice. These findings identify miR-96 and miR-183 as regulators of neovascularisation following MI and miR-regulated genes such as anillin as potential therapeutic targets for cardiovascular disease.
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