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. 2011 Jun 20;108(27):11193–11198. doi: 10.1073/pnas.1019536108

Fig. 2.

Fig. 2.

The miR-155 target SHIP-1 is down-regulated in RA SF CD14+ cells and in RA synovial tissue macrophages. (A) miR-155 regulates expression of SHIP-1 in RA PB and SF CD14+ cells. Cells were transfected with miR-155 mimic or antagomir or with appropriate controls as described in Fig. 1. Quantitative analysis of SHIP-1 mRNA expression is shown (n = 3). (B) miR-155 binds directly to the 3′ UTR of human SHIP-1 mRNA. pMir-hSHIP1 (sense) and pMir-hSHIP1 (antisense) 3′ UTR luciferase plasmids were cotransfected with control or miR-155 mimic (40 nM) in HEK293 cells. Luciferase activity was analyzed at 24 h. (C) Expression of SHIP-1 in paired PB and SF CD14+ cells from RA patients (n = 6). Data are means ± SEM. *P < 0.05. (D and E) Synovial specimens from RA (n = 5) and OA (n = 5) patients stained with anti-human SHIP-1 (D, brown) and counterstained with anti-CD68 antibody (E). Representative staining of one of five specimens is shown; blue, DAPI; red, CD68+; green, SHIP-1+; yellow, CD68+/SHIP-1+. (Magnification: 63×.) Enlargements in E show a SHIP-1+ cell (green). Cont, control mimic; hSHIP-1, human SHIP-1; miR155antg, miR-155 antagomir; miR155m, miR-155 mimic; Cont antg, control antagomir. Relative luciferase activity is the maximal activity in the presence of pMiR plasmid alone.