miR-22 controls Irf8 mRNA abundance and murine dendritic cell development.
miR-22 controls Irf8 mRNA abundance and murine dendritic cell development.
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DOI:
10.1371/journal.pone.0052341
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Watowich SS
中科院分区:
文献类型:
--
作者:
Li HS;Greeley N;Sugimoto N;Liu YJ;Watowich SS
MicroRNAs (miRNAs) have emerged as critical regulators of many cellular responses, through the action of miRNA-induced silencing complex (miRISC)- or miRNA ribonucleoprotein complex (miRNP)-mediated gene repression. Here we studied the role of miRNAs in the development of dendritic cells (DCs), an important immune cell type that is divided into conventional DC (cDC) and plasmacytoid DC (pDC) subsets. We found that miR-22 was highly expressed in mouse CD11c+ CD11b+ B220− cDCs compared to pDCs, and was induced in DC progenitor cell cultures with GM-CSF, which stimulate CD11c+ CD11b+ B220− cDC differentiation. Enforced overexpression of miR-22 during DC development enhanced CD11c+ CD11b+ B220− cDC generation at the expense of pDCs, while miR-22 knockdown demonstrated opposite effects. Moreover, overexpression and knockdown of miR-22 showed significant effects on the mRNA abundance of Irf8, which encodes the transcription factor IRF8 that plays essential roles in DC development. Luciferase reporter assays confirmed that miR-22 binds directly to the 3′UTR of the mouse Irf8 mRNA. Collectively, these results suggest that miR-22 targets Irf8 mRNA for posttranscriptional repression and controls DC subset differentiation.
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DOI:
10.1084/jem.20061692
发表时间:
2006-10-30
期刊:
The Journal of experimental medicine
影响因子:
--
作者:
Cobb BS;Hertweck A;Smith J;O'Connor E;Graf D;Cook T;Smale ST;Sakaguchi S;Livesey FJ;Fisher AG;Merkenschlager M
通讯作者:
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影响因子:
4
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通讯作者:
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影响因子:
64.8
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通讯作者:
Camargo, Fernando D.
影响因子:
13.6
作者:
Carissimi, Claudia;Fulci, Valerio;Macino, Giuseppe
通讯作者:
Macino, Giuseppe
影响因子:
20.3
作者:
Hashimi, Sara T.;Fulcher, Jennifer A.;Lee, Benhur
通讯作者:
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