MicroRNA-155 is induced during the macrophage inflammatory response

O’Connell, Ryan M.; Taganov, Konstantin D.; Boldin, Mark; Cheng, Genhong; Baltimore, David

doi:10.1073/pnas.0610731104

Cited by 1,679 publications

(1,560 citation statements)

References 47 publications

Supporting

Mentioning

1,475

Contrasting

Unclassified

Order By: Relevance

“…We demonstrated that IFN-␣/␤ treatment of monocytes induced the expression of anti-HIV miRNAs ( Figure 2C). This finding supports the studies by others 36,43,44 showing that IFN-␣/␤ is the potent inducer of miRNAs in several cell systems. However, this IFN-mediated anti-HIV innate immunity in monocytes was dampened by morphine treatment (Figure 2C).…”

Section: Discussionsupporting

confidence: 92%

Inhibition of Anti-HIV MicroRNA Expression

Wang

Zhou

et al. 2011

The American Journal of Pathology

View full text Add to dashboard Cite

Several micro RNAs (miRNAs) have the ability to inhibit HIV replication in target cells. Thus, we investigated the impact of opioids (morphine and heroin), widely abused drugs among people infected with HIV, on the expression of cellular anti-HIV miRNAs in monocytes. We found that morphine-treated monocytes expressed lower levels of cellular anti-HIV miRNAs than untreated cells. In addition, morphine treatment of monocytes compromised type I interferon (IFN)-induced anti-HIV miRNA expression. These findings paralleled the observation that morphine treatment of monocytes enhanced HIV replication. These morphine-mediated actions on the anti-HIV miRNAs and HIV could be antagonized by the opioid receptor antagonists (naltrexone or Cys2, Tyr3, Arg5, Pen7-amide). Furthermore, the in vitro impact of morphine on miRNA expression was confirmed by the in vivo observation that heroin-dependent subjects had significantly lower levels of anti-HIV miRNAs (miRNA-28, 125b, 150, and 382) in peripheral blood mononuclear cells than the healthy subjects. These in vitro and in vivo findings indicate that opioid use impairs intracellular innate anti-HIV mechanism(s) in monocytes, contributing to cell susceptibility to HIV infection. (Am J

show abstract

Section: Discussionsupporting

confidence: 92%

Inhibition of Anti-HIV MicroRNA Expression

Wang

Zhou

et al. 2011

The American Journal of Pathology

View full text Add to dashboard Cite

show abstract

“…Murine macrophages up-regulate miR-155 after exposure to poly(I-C) and TNF␣ (38), whereas human monocytes increase miR-146a after LPS stimulation (29). We found increased levels of miR-155 in monocytes derived from the synovial fluid of RA patients as compared with those derived from the RA peripheral blood.…”

Section: Discussionmentioning

confidence: 62%

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis

Stańczyk

Pedrioli

Brentano

et al. 2008

Arthritis & Rheumatism

756

624

View full text Add to dashboard Cite

Objective. MicroRNAs (miRNA) have recently emerged as a new class of modulators of gene expression. In this study we investigated the expression, regulation, and function of miR-155 and miR-146a in rheumatoid arthritis (RA) synovial fibroblasts (RASFs) and RA synovial tissue.Methods. Locked nucleic acid microarray was used to screen for differentially expressed miRNA in RASFs treated with tumor necrosis factor ␣ (TNF␣). TaqMan-based real-time polymerase chain reaction was applied to measure the levels of miR-155 and miR-146a. Enforced overexpression of miR-155 was used to investigate the function of miR-155 in RASFs.Results

show abstract

“…This adds to the growing evidence of the role of MAP kinases and their downstream transcription factor targets in the regulation of miR (O'Connell et al, 2007;Rahadiani et al, 2008). In addition, BCR activation induces miR-155 through ERK and JNK but not p38 activation through a conserved AP-1 element .…”

Section: Ebv Lmp1 Regulates Tcl1 Through Mir-29bmentioning

confidence: 70%

Epstein–Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b

et al. 2009

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) is noted for its transforming potential. Yet, it also acts as a cytostatic and growth-relenting factor in Burkitt's lymphoma (BL) cells. The underlying molecular mechanisms of the growth inhibitory property of LMP1 have remained largely unknown. In this study, we show that LMP1 negatively regulates a major oncogene, TCL1, in diffuse large B-cell lymphoma (DLBCL) and BL cells. MicroRNA (miR) profiling of LMP1 transfectants showed that among others, miR-29b, is upregulated. LMP1 diminished TCL1 by inducing miR29b through C-terminus activation region 1 (CTAR1) and CTAR2. miR-29b locked nucleic acid (LNA) antisense oligonucleotide transfection into LMP1-expressing cells reduced miR-29b expression and consequently reconstituted TCL1, suggesting that LMP1 negatively regulates TCL1 through miR-29b upregulation. The miR-29b increase by LMP1 was due to an increase in the cluster pri-miR-29b1-a transcription, derived from human chromosome 7. Using pharmacological inhibitors, we found that p38 mitogen-activated protein kinase-activating function of LMP1 is important for this effect. The ability of LMP1 to negatively regulate TCL1 through miR-29b might underlie its B-cell lymphoma growth antagonistic property. As LMP1 is also important for B-cell transformation, we suggest that the functional dichotomy of this viral protein may depend on a combination of levels of its expression, lineage and differentiation of the target cells and regulation of miRs, which then directs the outcome of the cellular response.

show abstract

MicroRNA-155 is induced during the macrophage inflammatory response

Cited by 1,679 publications

References 47 publications

Inhibition of Anti-HIV MicroRNA Expression

Inhibition of Anti-HIV MicroRNA Expression

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis

Epstein–Barr virus encoded LMP1 downregulates TCL1 oncogene through miR-29b

Contact Info

Product

Resources

About