Regulation of Monocyte Functional Heterogeneity by miR-146a and Relb
Name
Etzrodt-2012-Regulation of Monocy.pdf
Size
1.3 MB
Format
Adobe PDF
Checksum (MD5)
ed482a4f3f6a083444825b9ec26fb637
Author(s) • • • • • • • • •
Etzrodt, Martin
Cortez-Retamozo, Virna
Newton, Andita
Zhao, Jimmy
Ng, Aylwin C. Y.
Wildgruber, Moritz
Romero, Pedro
Wurdinger, Thomas
Xavier, Ramnik
Geissmann, Frederic
Date Issued
April 2012
Journal
Cell Reports
Publisher
Elsevier
Citation
Etzrodt, Martin, Virna Cortez-Retamozo, Andita Newton, Jimmy Zhao, Aylwin Ng, Moritz Wildgruber, Pedro Romero, et al. “Regulation of Monocyte Functional Heterogeneity by miR-146a and Relb.” Cell Reports 1, no. 4 (April 2012): 317–324.
Version
Final published version
Abstract
Monocytes serve as a central defense system against infection and injury but can also promote pathological inflammatory responses. Considering the evidence that monocytes exist in at least two subsets committed to divergent functions, we investigated whether distinct factors regulate the balance between monocyte subset responses in vivo. We identified a microRNA (miRNA), miR-146a, which is differentially regulated both in mouse (Ly-6C[superscript hi]/Ly-6C[superscript lo]) and human (CD14[superscript hi]/CD14[superscript lo]CD16[superscript +]) monocyte subsets. The single miRNA controlled the amplitude of the Ly-6C[superscript hi] monocyte response during inflammatory challenge whereas it did not affect Ly-6C[superscript lo] cells. miR-146a-mediated regulation was cell-intrinsic and depended on Relb, a member of the noncanonical NF-κB/Rel family, which we identified as a direct miR-146a target. These observations not only provide mechanistic insights into the molecular events that regulate responses mediated by committed monocyte precursor populations but also identify targets for manipulating Ly-6C[superscript hi] monocyte responses while sparing Ly-6C[superscript lo] monocyte activity.
MIT Department
Institute for Medical Engineering and Science
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/j.celrep.2012.02.009