Fig. 2

The PI3K/Akt signaling pathway was required for MSC proliferation induced by omentin-1. To determine the role of the PI3K/Akt signaling pathway in the proliferative actions of omentin-1, cells were pretreated with LY294002 (LY; 20 μm/L) before omentin-1 (800 ng/ml) treatment for 1 h. For the cell cycle assay and EdU assay, MSCs were treated with omentin-1 (0–800 ng/ml) with or without LY294002 for 5 days. a,b The cell cycle was evaluated using flow cytometry. c,d 5-Ethynyl-2’-deoxyuridine (EdU) assay showed that a blockade of PI3K/Akt could reduce omentin-1-mediated MSC proliferation. e Growth curve of MSCs after omentin-1 (0–800 ng/ml) intervention from days 1 to 7 with or without LY294002. f–h After treatment with omentin-1 (800 ng/ml) for 5 days, the protein expression levels of cyclin D1, cyclin E, p21, and p27 were markedly changed; however, they were abolished by pretreatment with LY294002. Data are presented as the mean ± SD of three separate experiments. *P < 0.05, versus the control group; ^# P < 0.05, versus the 800 ng/ml omentin-1 treated group. Cont. control, OD optical density