Fig 2: MTRN localization in non-human primate retina flat-mount. Immunostaining on the flat-mount retina of MTRN (green), TSP1 (red), and GS (red). MTRN and TSP1 are highly concentrated around the optic nerve head (NO = Optic Nerve), and co-localize at the macula and around the fovea* (a). Colocalization of MTRN with GS expressed in Müller cells at the macula (b and inset).

Fig 3: MT1-MMP absence in endothelial cells leads to perivascular accumulation of thrombospondin-1 (TSP1) in the inflamed colon A, BRepresentative maximum-intensity projection images of staining for TSP1 (red) and CD31 (gray) in (A) and also for MT1-MMP (green) in (B) in colon sections obtained from MT1f/f and MT1i?EC mice left untreated (A) or treated with 1% DSS for 3 days (B). Magnified views are shown to the right. Scale bars, 100 µm in main panels and 10 µm in the magnified views.CTSP1 mean fluorescence intensity (MFI) in the perivascular area of large vessels present in the colon mucosa of treated mice, as depicted in (B); n = 4 mice per genotype. Data are shown as mean ± SEM and were tested by t-test; *P < 0.05.Data information: Please see Appendix Table S3 for exact P-values.Source data are available online for this figure.

Fig 4: NF-?B dependence of miRNA expression changes. (A) Analysis of the presence of NF-?B subunit binding motifs (from TRANSFAC database) in a 1,000-bp window centered around the estimated TSS of the miRNAs. (B) ChIP assays for selected miRNAs showing the binding of NF-?B p65 near the TSS 2 and 4 days after RANKL/M-CSF stimulation of MOs. Each graph contains the relative enrichment of samples immunoprecipitated with the anti-p65 antibody and an IgG as a control. MO samples were tested at 0, 2 and 4 days after M-CSF/RANKL stimulation. On top of each graph the sequence analyzed is indicated. p65 putative binding sites are indicated with a blue dot. Primers used for amplification are indicated with arrows around p65 binding sites. (C) Effects of the two NF-?B inhibitors (10 µM BAY 11-7082 (BAY11) and 100 µM sodium aurothiomalate (SATM) on the phosphorylation levels of p65 as determined by western blotting. p65 and H3 total levels are used as controls. (D) Effects of two NF-?B inhibitors (BAY11 and SATM) on the levels of miRNAs within the miR-99b/125a/let7e and miR-132/212 clusters measured by a time-course analysis of MOs stimulated with RANKL/M-CSF. (E) Effects of treatment with BAY11 and SATM on markers of OC differentiation (ACP5, CTSK, TM7SF4, MMP9) as estimated by qRT-PCR. Data relative to DMSO-treated samples and normalized with RPL38 expression levels. (F) Effects of treatment with BAY 11 and SATM on miRNA targets (IGF1R, TNFAIP3, ITGA4, THBS, IL15 and PTGS2) as estimated by qRT-PCR. Data are relative to DMSO-treated samples and are normalized with respect to RPL38 expression levels. Error bars correspond to the standard deviation of three independent measurements; *corresponds to P-value <0.05; **means P-value <0.01.

Fig 5: In vitro cold stress exposure increases RBM3 and thrombospondin-1 protein expression in mouse vastus lateralis muscle biopsies. (A) Representative immunoblots for the cellular expression of the cold-shock RNA-binding motif 3 protein (RBM3) in mouse vastus lateralis muscle fragments (EMI assay) incubated for 24 h in vitro at 37°C or 28°C. ß-actin was used as a loading control. (B) Representative immunoblots and densitometry analysis of thrombospondin-1 (THBS-1) protein expression in these same muscle samples. ß-actin was used as a loading control. Significant difference between 37°C and 28°C: *, p = 0.05 (data represented are means ± SEM from n = 6 samples).