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O-Glycosylation with O-linked β-N-acetylglucosamine increases vascular contraction: Possible modulatory role on Interleukin-10 signaling pathway

Miguez, Jéssica S.G. ; Dela Justina, Vanessa ; Bressan, Alecsander F.M. ; Marchi, Patrícia G.F. ; Honorio-França, Adenilda C. ; Carneiro, Fernando S. ; Clinton Webb, R. ; Tostes, Rita C. ; Giachini, Fernanda R. ; Lima, Victor V.

Life sciences (1973), 2018-09, Vol.209, p.78-84 [Periódico revisado por pares]

Netherlands: Elsevier Inc

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  • Título:
    O-Glycosylation with O-linked β-N-acetylglucosamine increases vascular contraction: Possible modulatory role on Interleukin-10 signaling pathway
  • Autor: Miguez, Jéssica S.G. ; Dela Justina, Vanessa ; Bressan, Alecsander F.M. ; Marchi, Patrícia G.F. ; Honorio-França, Adenilda C. ; Carneiro, Fernando S. ; Clinton Webb, R. ; Tostes, Rita C. ; Giachini, Fernanda R. ; Lima, Victor V.
  • Assuntos: Aorta ; Arteries ; Contraction ; Cytokine ; Cytokines ; Diabetes mellitus ; ERK 1/2 ; Glycosylation ; Hypertension ; Interleukin 10 ; Interleukins ; Janus kinase ; N-Acetylglucosamine ; O-GlcNAc ; O-GlcNAcylation ; Phosphorylation ; Post-translation ; Proteins ; Signal transduction ; Signaling ; Stat3 protein ; Vascular dysfunction
  • É parte de: Life sciences (1973), 2018-09, Vol.209, p.78-84
  • Notas: ObjectType-Article-2
    SourceType-Scholarly Journals-1
    ObjectType-Feature-3
    content type line 23
    ObjectType-Review-1
  • Descrição: The interleukin-10 (IL-10) is an immuno-regulatory cytokine that plays a protective effect in the vasculature. IL-10 binding to its receptor, activating the IL-10/JAK1/STAT3 cascade to exert its effects. Therefore, STAT3 phosphorylation is essential for IL-10 actions. O-Glycosylation with linked β-N-acetylglucosamine (O-GlcNAc) is a post-translational modification able to regulate many proteins by interfering with protein on a phosphorylation level. Our aim was to determine whether O-GlcNAc promotes the inhibition of IL-10-pathway (JAK1/STAT3/IL-10), inactivationg its action in the vasculature. Mice (C57BL/6) aortic segments were incubated with vehicle or Thiamet G (0.1 mM, for 24 h) to increase global O-GlcNAc levels. Aortas from knockout mice for IL-10 were also used. Vascular reactivity and western blot tests were performed to evaluate protein expression. High levels of O-GlcNAc, induced by Thiamet G incubation, increased vascular expression of JAK1, but decreased expression and activity of STAT3. In addition, IL-10 levels were diminished in arteries treated with Thiamet G. Absence of IL-10, as well as augmented O-GlcNAcylation, increased vascular reactivity to constrictor stimuli, an effect that was abolished by ERK 1/2 inhibitor. High levels of O-GlcNAc and the absence of IL-10 also leads to increased vascular expression of ERK1/2. Our data suggest that O-GlcNAc modification seems to (dys)regulate IL-10 signaling pathway and consequently, compromise the protective effect of this cytokine in vasculature. It is possible that there is a promising relationship in pathophysiological conditions where changes in O-GlcNAcylation and IL-10 levels are observed, such as hypertension and diabetes. [Display omitted]
  • Editor: Netherlands: Elsevier Inc
  • Idioma: Inglês
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