miR-27b*, an Oxidative Stress-Responsive microRNA Modulates Nuclear Factor-kB Pathway in RAW 264.7 Cells

Authors

Sivasubramani Thulasingam, University of Nebraska - Lincoln
Chandirasegaran Massilamany, University of Nebraska-LincolnFollow
Arunakumar Gangaplara, University of Nebraska - Lincoln
Hongjiu Dai, University of Nebraska - Lincoln
Shahlo Yarbaeva, University of Nebraska - Lincoln
Sakthivel Subramaniam, University of Nebraska - Lincoln
Jean-Jack Riethoven, University of Nebraska - LincolnFollow
James Eudy, University of Nebraska Medical CenterFollow
Marjorie F. Lou, University of Nebraska - LincolnFollow
Jay Reddy, University of Nebraska - LincolnFollow

Document Type

Article

Date of this Version

2011

Citation

Published in Molecular and Cellular Biochemistry (2011) 352: 181-188. DOI: 10.1007/s11010-011-0752-2.

Comments

Copyright 2011, Springer. Used by permission.

Abstract

Reactive oxygen species (ROS) produced in macrophages is critical for microbial killing, but they also take part in inflammation and antigen presentation functions. MicroRNAs (miRNAs) are endogenous regulators of gene expression, and they can control immune responses. To dissect the complex nature of ROS-mediated effects in macrophages, we sought to characterize miRNAs that are responsive to oxidative stress-induced with hydrogen peroxide (H₂O₂) in the mouse macrophage cell line, RAW 264.7. We have identified a set of unique miRNAs that are differentially expressed in response to H₂O₂. These include miR-27a*, miR-27b*, miR-29b*, miR-24-2*, and miR21*, all of which were downregulated except for miR-21*. By using luciferase reporter vector containing nuclear factor-kB (NF-kB) response elements, we demonstrate that overexpression of miR-27b* suppresses lipopolysaccharide-induced activation of NF-kB in RAW 264.7 cells. Our data suggest that macrophage functions can be regulated by oxidative stress-responsive miRNAs by modulating the NF-kB pathway.