Figure 2.

Effects of UC-MSCs on FLSs proliferation. (a) Compared with the control, TNF-α (20 ng/ml) significantly induced the proliferation of FLSs after five days of culture. UC-MSCs inhibited TNF-α-stimulated-FLSs proliferation in a dose-dependent fashion in the cell-to-cell contact system and also the transwell system. All the data are expressed as the mean ± SD of more than three independent experiments. **P < 0.01 vs. the controls. (b) FLSs proliferation was significantly inhibited when UC-MSCs were added on the fourth day after the initiation of stimulation in the five-day coculture experiment. All the data are expressed as the mean ± SD of more than three independent experiments. **P < 0.01 vs. the control. (c) Anti-IL-10, 1-MT and anti-TGF-β1 restored FLSs proliferation. FLSs (1 × 104) were activated with TNF-α in the presence or absence of irradiated MSCs (1 × 104) in 96-well plates. Anti-IL-10 (10 μg/Ml), 1-MT (1 mM) and TGF-β1 antibody (10 μg/mL) were added for five days. The incorporation of (3H)-thymidine is shown by CPM. All the data are expressed as the mean ± SD of more than three independent experiments. **P < 0.01.

Liu et al. Arthritis Research & Therapy 2010 12:R210   doi:10.1186/ar3187
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