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Targeting miR-181a/b in retinitis pigmentosa: implications for disease progression and therapy

Costa, Bruna Lopes da ; Quinn, Peter M J ; Wu, Wen-Hsuan ; Liu, Siyuan ; Nolan, Nicholas D ; Demirkol, Aykut ; Tsai, Yi-Ting ; Caruso, Salvatore Marco ; Cabral, Thiago ; Wang, Nan-Kai ; Tsang, Stephen H

Cell & bioscience, 2024-05, Vol.14 (1), p.64-64, Article 64 [Periódico revisado por pares]

England: BioMed Central Ltd

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  • Título:
    Targeting miR-181a/b in retinitis pigmentosa: implications for disease progression and therapy
  • Autor: Costa, Bruna Lopes da ; Quinn, Peter M J ; Wu, Wen-Hsuan ; Liu, Siyuan ; Nolan, Nicholas D ; Demirkol, Aykut ; Tsai, Yi-Ting ; Caruso, Salvatore Marco ; Cabral, Thiago ; Wang, Nan-Kai ; Tsang, Stephen H
  • Assuntos: Aerobic glycolysis ; Health aspects ; Metabolic reprogramming ; MicroRNA ; MicroRNAs ; Retinal pigment epithelium ; Retinitis pigmentosa ; Scientific equipment and supplies industry
  • É parte de: Cell & bioscience, 2024-05, Vol.14 (1), p.64-64, Article 64
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Retinitis pigmentosa (RP) is a genetically heterogeneous group of degenerative disorders causing progressive vision loss due to photoreceptor death. RP affects other retinal cells, including the retinal pigment epithelium (RPE). MicroRNAs (miRs) are implicated in RP pathogenesis, and downregulating miR-181a/b has shown therapeutic benefit in RP mouse models by improving mitochondrial function. This study investigates the expression profile of miR-181a/b in RPE cells and the neural retina during RP disease progression. We also evaluate how miR-181a/b downregulation, by knocking out miR-181a/b-1 cluster in RPE cells, confers therapeutic efficacy in an RP mouse model and explore the mechanisms underlying this process. Our findings reveal distinct expression profiles, with downregulated miR-181a/b in RPE cells suggesting a protective response and upregulated miR-181a/b in the neural retina indicating a role in disease progression. We found that miR-181a/b-2, encoded in a separate genomic cluster, compensates for miR-181a/b-1 ablation in RPE cells at late time points. The transient downregulation of miR-181a/b in RPE cells at post-natal week 6 (PW6) led to improved RPE morphology, retarded photoreceptor degeneration and decreased RPE aerobic glycolysis. Our study elucidates the underlying mechanisms associated with the therapeutic modulation of miR-181a/b, providing insights into the metabolic processes linked to its RPE-specific downregulation. Our data further highlights the impact of compensatory regulation between miR clusters with implications for the development of miR-based therapeutics.
  • Editor: England: BioMed Central Ltd
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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