Fig. 2

miR-200c is upregulated in macrophages upon M1 polarization and its inhibition decreases M1 genes. a BMDM were polarized towards M1 and M2 phenotype by LPS (10 ng/ml) and IL-4 (20 ng/ml), respectively, and compared to untreated (UT) macrophages. Total RNA was extracted and miR-200c levels were measured by RT-qPCR. MiR-200c was increased in M1 and decreased in M2 macrophages (N = 6; **p < 0.01; ***p < 0.001). b, c, d BMDM were treated with LNA anti miR-scramble (scr) or anti-miR-200c (1 μM) for 24 h, stimulated with LPS (10 ng/ml) for 2 h and compared to unstimulated macrophages. Then total RNA was extracted. b miR-200c levels were measured by RT-qPCR in total RNA extracted from BMDM. miR-200c was strongly decreased by LNA anti-miR-200c treatment both under basal and LPS treatment (N = 3; *p < 0.05; **p < 0.01). c RT-qPCR of a miR-200c target gene, SIRT1, that was increased in BMDM anti-miR-200c treated cells, both under basal and LPS treatment (N = 4; *p < 0.05; **p < 0.01). d RT-qPCR of M1-inflammatory genes: TNFα L-6, IL-1β, iNOS. All M1 genes were induced by LPS treatment and were decreased by anti-miR-200c in LPS treated BMDM (N = 3–4; *p < 0.05; **p < 0.01; ***p < 0,001)