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. 2017 Oct 16;8:1327. doi: 10.3389/fimmu.2017.01327

Figure 3.

Figure 3

miR-148a-3p can promote M1 and inhibit M2 macrophage polarization. (A) BM-derived macrophages (BMDMs) were polarized with PBS (M0), lipopolysaccharide (LPS) + interferon (IFN)-γ (M1), or interleukin (IL)-4 (M2). The relative level of miR-148a-3p in monocytes and polarized BMDMs was determined by qRT-PCR, using U6 RNA as a reference control (n = 3). (B) BMDMs were transfected with miR-148a-3p mimic or N.C. Cells were then polarized with PBS (M0), LPS + IFN-γ (M1), or IL-4 (M2) for 24 h. The mRNA levels of iNos, Il6, Tnf-α, and Mr were determined by qRT-PCR, using β-actin (ACTB) as a reference control (n = 3). (C) BMDMs were transfected with miR-148a-3p inhibitor or N.C. Cells were then polarized with PBS (M0), LPS + IFN-γ (M1), or IL-4 (M2). The mRNA levels of iNos, Il6, Tnf-α, and Mr were determined by qRT-PCR, using β-actin as a reference control (n = 3). (D,E) BMDMs from (A) were irradiated and cocultured with carboxyfluorescein diacetatesuccinimidyl ester (CFSE)-labeled allogeneic T cells for 24 h. The proliferation of T cells was determined by FACS (D) and compared among treatment groups (E) (n = 6). Bars, mean ± SD; *P < 0.05; **P < 0.01; ***P < 0.001.