Papers

Peer-reviewed International journal
Feb 3, 2011

miR-155, a Modulator of FOXO3a Protein Expression, Is Underexpressed and Cannot Be Upregulated by Stimulation of HOZOT, a Line of Multifunctional Treg.

PloS one
  • Mayuko Yamamoto
  • ,
  • Eisaku Kondo
  • ,
  • Makoto Takeuchi
  • ,
  • Akira Harashima
  • ,
  • Takeshi Otani
  • ,
  • Kazue Tsuji-Takayama
  • ,
  • Fumiyuki Yamasaki
  • ,
  • Hiromi Kumon
  • ,
  • Masayoshi Kibata
  • ,
  • Shuji Nakamura

Volume
6
Number
2
First page
e16841
Last page
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1371/journal.pone.0016841

MicroRNAs (miRNAs) play important roles in regulating post-transcriptional gene repression in a variety of immunological processes. In particular, much attention has been focused on their roles in regulatory T (Treg) cells which are crucial for maintaining peripheral tolerance and controlling T cell responses. Recently, we established a novel type of human Treg cell line, termed HOZOT, multifunctional cells exhibiting a CD4(+)CD8(+) phenotype. In this study, we performed miRNA profiling to identify signature miRNAs of HOZOT, and therein identified miR-155. Although miR-155 has also been characterized as a signature miRNA for FOXP3(+) natural Treg (nTreg) cells, it was expressed quite differently in HOZOT cells. Under both stimulatory and non-stimulatory conditions, miR-155 expression remained at low levels in HOZOT, while its expression in nTreg and conventional T cells remarkably increased after stimulation. We next searched candidate target genes of miR-155 through bioinformatics, and identified FOXO3a, a negative regulator of Akt signaling, as a miR-155 target gene. Further studies by gain- and loss-of-function experiments supported a role for miR-155 in the regulation of FOXO3a protein expression in conventional T and HOZOT cells.

Link information
DOI
https://doi.org/10.1371/journal.pone.0016841
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/21304824
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033424
ID information
  • DOI : 10.1371/journal.pone.0016841
  • Pubmed ID : 21304824
  • Pubmed Central ID : PMC3033424

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