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Control of the Inflammatory Macrophage Transcriptional Signature by miR-155

Jablonski, Kyle A., Gaudet, Andrew D., Amici, Stephanie A., Popovich, Phillip G., Guerau-de-Arellano, Mireia·2016·PLOS ONE
DOI 10.1371/journal.pone.0159724PMC PMC4957803
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Fig 1 miR-155 is associated with the classically activated macrophage phenotype. Expression of miRNAs was determined by Taqman Real-Time PCR and expressed as mean relative expression (+ SEM) in (A) macrophages stimulated in vitro for 24 hours in M0, M1, and M2 (n = 3) conditions; expression relative to M0 condition; Post-hoc ANOVA, **p<0.005. (B) M1 and M2 macrophages activated in vitro over a 48 hour period; expression relative to 0 hour pre-stimulation time-point. Unpaired t-test, ***p<0.001. Results reproduced in two independent experiments.
Fig 1 miR-155 is associated with the classically activated macrophage phenotype. Expression of miRNAs was determined by Taqman Real-Time PCR and expressed as mean relative expression (+ SEM) in (A) macrophages stimulated in vitro for 24 hours in M0, M1, and M2 (n = 3) conditions; expression relative to M0 condition; Post-hoc ANOVA, **p<0.005. (B) M1 and M2 macrophages activated in vitro over a 48 hour period; expression relative to 0 hour pre-stimulation time-point. Unpaired t-test, ***p<0.001. Results reproduced in two independent experiments.CC BY · PubMed Central
Fig 2 Reduced classically activated M1 marker expression in miR-155 knock-out (KO) macrophages. (A) Inducible nitric oxide synthase (Nos2), (B) IL1b, (C) Tumor Necrosis Factor-α (Tnfa) (H) and Arginase-1 (Arg1) expression was determined by Real-Time PCR in wild-type (WT, n = 8–11) and miR-155 knockout (KO n = 8–12) bone marrow-derived macrophages in vitro activated in M1 or M2 conditions for 24 hours in three independent experiments. Gene expression is expressed as a percentage +/- SEM of the WT M1 condition. Unpaired t-test, *p<0.05, **p<0.005. Relative concentration of (D) nitric oxide (NO), (E) IL-1β protein and (F) TNF-α protein was determined using Griess assay (for NO) or Bio-Plex Suspension Array (For IL-1β and TNF-α) in cell lysates from WT (n = 5) and miR-155 KO (n = 5) bone marrow-derived macrophages in vitro activated in M1 or M2 conditions for 24 hours. Individual protein concentrations expressed as fraction of total protein concentration in either M0 or M1 condition. (G) IL1b expression was determined by Real-Time PCR in WT and KO bone marrow-derived macrophages transfected with a scrambled miR control (n = 5) or a miR-155 oligonucleotide mimic (n = 5) and activated in M0 (untreated), M1 (LPS+IFN-γ) or M2(IL-4) conditions for 24 hours. Gene expression is expressed as a percentage +/- SEM of the scrambled M1 condition. Unpaired t-test, ***p<0.0005, ****p<0.00005. (A-G) Data from 2–3 independent experiments.
Fig 2 Reduced classically activated M1 marker expression in miR-155 knock-out (KO) macrophages. (A) Inducible nitric oxide synthase (Nos2), (B) IL1b, (C) Tumor Necrosis Factor-α (Tnfa) (H) and Arginase-1 (Arg1) expression was determined by Real-Time PCR in wild-type (WT, n = 8–11) and miR-155 knockout (KO n = 8–12) bone marrow-derived macrophages in vitro activated in M1 or M2 conditions for 24 hours in three independent experiments. Gene expression is expressed as a percentage +/- SEM of the WT M1 condition. Unpaired t-test, *p<0.05, **p<0.005. Relative concentration of (D) nitric oxide (NO), (E) IL-1β protein and (F) TNF-α protein was determined using Griess assay (for NO) or Bio-Plex Suspension Array (For IL-1β and TNF-α) in cell lysates from WT (n = 5) and miR-155 KO (n = 5) bone marrow-derived macrophages in vitro activated in M1 or M2 conditions for 24 hours. Individual protein concentrations expressed as fraction of total protein concentration in either M0 or M1 condition. (G) IL1b expression was determined by Real-Time PCR in WT and KO bone marrow-derived macrophages transfected with a scrambled miR control (n = 5) or a miR-155 oligonucleotide mimic (n = 5) and activated in M0 (untreated), M1 (LPS+IFN-γ) or M2(IL-4) conditions for 24 hours. Gene expression is expressed as a percentage +/- SEM of the scrambled M1 condition. Unpaired t-test, ***p<0.0005, ****p<0.00005. (A-G) Data from 2–3 independent experiments.CC BY · PubMed Central
Fig 3 miR-155 inhibitor reduces M1 marker expression. (A) Inducible nitric oxide synthase (Nos2) and (B) Tumor Necrosis Factor (Tnfa) expression was determined by Real-Time PCR in wild-type bone marrow-derived macrophages in vitro activated in M0 or M1 conditions for 24 hours and transfected with a scrambled (n = 3) or a miR-155 oligonucleotide inhibitor (n = 3–4). Gene expression is expressed as a percentage +/- SEM of the scrambled M1 condition. Unpaired t-test, *p<0.05. Data reproduced in two independent experiments.
Fig 3 miR-155 inhibitor reduces M1 marker expression. (A) Inducible nitric oxide synthase (Nos2) and (B) Tumor Necrosis Factor (Tnfa) expression was determined by Real-Time PCR in wild-type bone marrow-derived macrophages in vitro activated in M0 or M1 conditions for 24 hours and transfected with a scrambled (n = 3) or a miR-155 oligonucleotide inhibitor (n = 3–4). Gene expression is expressed as a percentage +/- SEM of the scrambled M1 condition. Unpaired t-test, *p<0.05. Data reproduced in two independent experiments.CC BY · PubMed Central
Fig 4 Classically activated macrophage signature in wild-type and miR-155 knockout macrophages. Fold Change (FC) vs. Mean Expression Value (MEV) plot of microarray data highlighting 2 FC or higher up-regulated genes (red, p≤0.05) or down-regulated genes (blue, p≤0.05) in (A) knockout (KO) M1 to M0 macrophages comparison (n = 3). (B, C) FC vs. MEV plot with previously described classical M1 markers highlighted (in red) and the top 15 M1-exclusive genes (identified in [17]) most decreased in KO M1 macrophages (in green) in the WT M1 vs. M0 comparison (B) and the KO M1 vs. M0 comparison (C). Red lines represent a +/- 2FC cut-off.
Fig 4 Classically activated macrophage signature in wild-type and miR-155 knockout macrophages. Fold Change (FC) vs. Mean Expression Value (MEV) plot of microarray data highlighting 2 FC or higher up-regulated genes (red, p≤0.05) or down-regulated genes (blue, p≤0.05) in (A) knockout (KO) M1 to M0 macrophages comparison (n = 3). (B, C) FC vs. MEV plot with previously described classical M1 markers highlighted (in red) and the top 15 M1-exclusive genes (identified in [17]) most decreased in KO M1 macrophages (in green) in the WT M1 vs. M0 comparison (B) and the KO M1 vs. M0 comparison (C). Red lines represent a +/- 2FC cut-off.CC BY · PubMed Central
Fig 5 miR-155 is required for expression of the full classically activated macrophage signature. (A) Fold Change (FC) vs. Mean Expression Value (MEV) plot of knockout (KO) M1 vs. M0 microarray data, with highlighted classical wild-type (WT) M1 signature genes as defined in this study. Genes more than 2FC up-regulated in WT M1 macrophages (red genes in Fig 4A) are shown in red and genes more than 2FC down-regulated in WT M1 macrophages (blue genes in Fig 4A) are shown in blue. (B) WT M1/M0 FC vs. KO M1/M0 FC plot highlighting the WT M1 Up signature (in red) and WT M1 Down signature (in blue). The black line indicates the x = y trendline expected if all gene probes were similarly up- or down-regulated exactly the same in KO M1 and WT M1 macrophages (FC KO M1 vs KO M0 = FC WT M1 vs WT M0). The blue line indicates the power regression trendline that genes more closely adhered to, represented by y = 1.003x0.5956, R2 = 0.50052. (C) WT M1/M0 FC vs. KO M1/M0 FC plot highlighting classical M2 genes. Red lines represent a +/- 2FC cut-off. More than a single appearance of a gene symbol indicates different probes hybridizing the same gene transcript were present.
Fig 5 miR-155 is required for expression of the full classically activated macrophage signature. (A) Fold Change (FC) vs. Mean Expression Value (MEV) plot of knockout (KO) M1 vs. M0 microarray data, with highlighted classical wild-type (WT) M1 signature genes as defined in this study. Genes more than 2FC up-regulated in WT M1 macrophages (red genes in Fig 4A) are shown in red and genes more than 2FC down-regulated in WT M1 macrophages (blue genes in Fig 4A) are shown in blue. (B) WT M1/M0 FC vs. KO M1/M0 FC plot highlighting the WT M1 Up signature (in red) and WT M1 Down signature (in blue). The black line indicates the x = y trendline expected if all gene probes were similarly up- or down-regulated exactly the same in KO M1 and WT M1 macrophages (FC KO M1 vs KO M0 = FC WT M1 vs WT M0). The blue line indicates the power regression trendline that genes more closely adhered to, represented by y = 1.003x0.5956, R2 = 0.50052. (C) WT M1/M0 FC vs. KO M1/M0 FC plot highlighting classical M2 genes. Red lines represent a +/- 2FC cut-off. More than a single appearance of a gene symbol indicates different probes hybridizing the same gene transcript were present.CC BY · PubMed Central
Fig 6 miR-155 dependent M1 signature transcriptional networks. (A). Model of molecules involved in miR-155 dependent M1 activated transcriptional networks, identified by Ingenuity Pathway Analysis. miR-155-dependent M1 genes up-regulated more than 2 Fold Change (FC) in wild-type (WT) M1vs. WT M0 macrophages that were up-regulated to a lesser extent in knockout (KO) M1 vs. KO M0 macrophages are highlighted in red.
Fig 6 miR-155 dependent M1 signature transcriptional networks. (A). Model of molecules involved in miR-155 dependent M1 activated transcriptional networks, identified by Ingenuity Pathway Analysis. miR-155-dependent M1 genes up-regulated more than 2 Fold Change (FC) in wild-type (WT) M1vs. WT M0 macrophages that were up-regulated to a lesser extent in knockout (KO) M1 vs. KO M0 macrophages are highlighted in red.CC BY · PubMed Central
Fig 7 Identification of candidate miR-155 targets associated with M1 phenotype. (A) Fold Change (FC) vs. Mean Expression Value (MEV) plot of knockout (KO) M1 vs. wild-type (WT) M1 microarray data with miR-155 targets (high or moderate predicted targets and experimentally observed targets) that were down-regulated ≥2FC in WT M1 vs. WT M0 highlighted in red. 18 target genes were up-regulated more than 2 FC in KO M1 vs. KO M0. (B) Hierarchical clustering analysis of WT M0, WT M1, KO M0 and KO M1 samples based on expression of miR-155, IPA identified miR-155 dependent M1 Up genes from Fig 6 and top 18 miR-155 targets identified in (A). (C) Inpp5d, (D) Mafb, (E) Tspan14, and (F) Bat5 expressions were determined by Real-Time PCR in wild-type (WT, n = 3) and miR-155 knockout (KO n = 3) bone marrow-derived macrophages in vitro activated in M1 or M2 conditions for 24 hours. Data shown is representative of 2–3 independent experiments. Gene expression is expressed as a percentage +/- SEM of the WT M0 condition. Unpaired t-test, *p<0.05, **p<0.005. (F)
Fig 7 Identification of candidate miR-155 targets associated with M1 phenotype. (A) Fold Change (FC) vs. Mean Expression Value (MEV) plot of knockout (KO) M1 vs. wild-type (WT) M1 microarray data with miR-155 targets (high or moderate predicted targets and experimentally observed targets) that were down-regulated ≥2FC in WT M1 vs. WT M0 highlighted in red. 18 target genes were up-regulated more than 2 FC in KO M1 vs. KO M0. (B) Hierarchical clustering analysis of WT M0, WT M1, KO M0 and KO M1 samples based on expression of miR-155, IPA identified miR-155 dependent M1 Up genes from Fig 6 and top 18 miR-155 targets identified in (A). (C) Inpp5d, (D) Mafb, (E) Tspan14, and (F) Bat5 expressions were determined by Real-Time PCR in wild-type (WT, n = 3) and miR-155 knockout (KO n = 3) bone marrow-derived macrophages in vitro activated in M1 or M2 conditions for 24 hours. Data shown is representative of 2–3 independent experiments. Gene expression is expressed as a percentage +/- SEM of the WT M0 condition. Unpaired t-test, *p<0.05, **p<0.005. (F)CC BY · PubMed Central

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Authors
Jablonski, K. A., Gaudet, A. D., Amici, S. A., Popovich, P. G., & Guerau-de-Arellano, M.
Venue
PLOS ONE
Publisher
Public Library of Science (PLoS)
Published
2016-07-22
Volume
11
Issue
7
Pages
e0159724
ISSN
1932-6203
DOI
10.1371/journal.pone.0159724
PMC
PMC4957803
Cited by
146
References
13
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • International Foundation for Research on Paraplegia (P 129)
  • National Institute of Neurological Disorders and Stroke (NIH R21 R21NS081413)
  • Ray W. Poppleton Endowment
  • Canadian Institutes of Health Research (CA) Postdoctoral Fellowship
  • Ohio State University Mayer's Undergraduate Summer Research Fellowship

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