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Cited by 150

Early miR-155 upregulation contributes to neuroinflammation in Alzheimer’s disease triple transgenic mouse model

Guedes, Joana R., Custódia, Carlos M., Silva, Ricardo J., de Almeida, Luís P., Pedroso de Lima, Maria C., Cardoso, Ana L.·2014·Human Molecular Genetics
DOI 10.1093/hmg/ddu348
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Abstract

MicroRNAs (miRNAs) have emerged as a class of small, endogenous, regulatory RNAs that exhibit the ability to epigenetically modulate the translation of mRNAs into proteins. This feature enables them to control cell phenotypes and, consequently, modify cell function in a disease context. The role of inflammatory miRNAs in Alzheimer's disease (AD) and their ability to modulate glia responses are now beginning to be explored. In this study, we propose to disclose the functional role of miR-155, one of the most well studied immune-related miRNAs in AD-associated neuroinflammatory events, employing the 3xTg AD animal model. A strong upregulation of miR-155 levels was observed in the brain of 12-month-old 3xTg AD animals. This event occurred simultaneously with an increase of microglia and astrocyte activation, and before the appearance of extracellular Aβ aggregates, suggesting that less complex Aβ species, such as Aβ oligomers may contribute to early neuroinflammation. In addition, we investigated the contribution of miR-155 and the c-Jun transcription factor to the molecular mechanisms that underlie Aβ-mediated activation of glial cells. Our results suggest early miR-155 and c-Jun upregulation in the 3xTg AD mice, as well as in Aβ-activated microglia and astrocytes, thus contributing to the production of inflammatory mediators such as IL-6 and IFN-β. This effect is associated with a miR-155-dependent decrease of suppressor of cytokine signaling 1. Furthermore, since c-Jun silenc…

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Crossref · 10.1093/hmg/ddu348

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  • MiR-155 is one of the strongest determinants of microglial pathogenicity; its upregulation in AD microglia enhances NF-κB signaling, increases production of pro-inflammatory cytokines, and reduces phagocytic Aβ clearance, thereby worsening plaque burden and neuronal injury.

    “MiR-155 is one of the strongest determinants of microglial pathogenicity. Its upregulation in AD microglia enhances NF-κB signaling, increases production of pro-inflammatory cytokines, and reduces phagocytic Aβ clearance, thereby worsening plaque burden and neuronal injury (Cardoso et al., 2011; Guedes et al., 2014).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Guedes et al., 2014

  • MiR-155 is induced in reactive astrocytes and is associated with pro-inflammatory glial reprogramming.

    “MiR-155 is also induced in reactive astrocytes and is associated with pro-inflammatory glial reprogramming.”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Guedes et al., 2014

  • Inhibition of miR-155 using antagomirs reduces microglial inflammatory activation and improves pathological outcomes in experimental AD models.

    “For example, inhibition of miR-155 using antagomirs has been shown to reduce microglial inflammatory activation and improve pathological outcomes in experimental AD models (Aloi et al., 2023; Guedes et al., 2014).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Guedes et al., 2014

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Authors
Guedes, J. R., Custódia, C. M., Silva, R. J., de Almeida, L. P., Pedroso de Lima, M. C., & Cardoso, A. L.
Venue
Human Molecular Genetics
Publisher
Oxford University Press (OUP)
Published
2014-07-02
Volume
23
Issue
23
Pages
6286-6301
ISSN
  • 0964-6906
  • 1460-2083
DOI
10.1093/hmg/ddu348
Cited by
150
References
14
Language
en

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