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http://purl.uniprot.org/citations/29474366http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29474366http://www.w3.org/2000/01/rdf-schema#comment"

Aims

CR6 interacting factor 1 (CRIF1) deficiency impairs mitochondrial oxidative phosphorylation complexes, contributing to increased mitochondrial and cellular reactive oxygen species (ROS) production. CRIF1 downregulation has also been revealed to decrease sirtuin 1 (SIRT1) expression and impair vascular function. Inhibition of SIRT1 disturbs oxidative energy metabolism and stimulates nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-induced inflammation. Therefore, we hypothesized that both CRIF1 deficiency-induced mitochondrial ROS production and SIRT1 reduction play stimulatory roles in vascular inflammation.

Methods and results

Plasma levels and mRNA expression of proinflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6) were markedly elevated in endothelium-specific CRIF1-knockout mice and CRIF1-silenced endothelial cells, respectively. Moreover, CRIF1 deficiency-induced vascular adhesion molecule-1 (VCAM-1) expression was consistently attenuated by the antioxidant N-acetyl-cysteine and NF-κB inhibitor (BAY11). We next showed that siRNA-mediated CRIF1 downregulation markedly activated NF-κB. SIRT1 overexpression not only rescued CRIF1 deficiency-induced NF-κB activation but also decreased inflammatory cytokines (TNF-α, IL-1β, and IL-6) and VCAM-1 expression levels in endothelial cells.

Conclusions

These results strongly suggest that CRIF1 deficiency promotes endothelial cell inflammation by increasing VCAM-1 expression, elevating inflammatory cytokines levels, and activating the transcription factor NF-κB, all of which were inhibited by SIRT1 overexpression."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0192693"xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Choi S."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Kim S.M."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Kim S."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Lee J.W."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Kim D.W."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Park J.B."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Lee I."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Lee Y.R."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Kim C.S."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Won M."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Irani K."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Jung S.B."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Lee S.D."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Jeon B.H."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Hur G.M."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Piao S."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Shin N."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/author"Nagar H."xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/pages"e0192693"xsd:string
http://purl.uniprot.org/citations/29474366http://purl.uniprot.org/core/title"CR6 interacting factor 1 deficiency promotes endothelial inflammation by SIRT1 downregulation."xsd:string
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