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. 2020 Jan 6;51:102615. doi: 10.1016/j.ebiom.2019.102615

Fig. 3.

Fig. 3

IL-1Ra mediates the functional improvement of human T2DM islets by MSCs. (A) GSI fold change of hT2DM islets with or without IL-1Ra treatment (1000 ng/mL) for 24 h. (B) Relative mRNA expression of FOXO1, NKX6.1, and MAFA in hT2DM islets with or without IL-1Ra treatment. (C) GSI fold change of hT2DM islets treated with MSCs coculture, MSCs coculture in the presence of neutralizing anti-IL-1Ra (nIL-1Ra, 500 ng/mL). (D) Relative mRNA expression of FOXO1, NKX6.1, MAFA in hT2DM islets treated with MSCs coculture, or MSCs coculture in the presence of neutralizing anti-IL-1Ra (nIL-1Ra, 500 ng /mL). (E) Relative mRNA expression of IL-1Ra in MSCs with IL-1Ra knockdown (MSC-KD) or control cells (MSC—NC). (F) GSI fold change of hT2DM islets cocultured with MSCs with negative control (+MSC—NC) or with IL-1Ra knockdown (+MSC-KD),or cultured alone. GSI of control group (hT2DM) was arbitrarily set to 1, and that of treatment groups were expressed as fold change compared with that of the control group. Data were shown as mean±SEM of 4 independent experiments with islets from 2 donors. *p<0.05, **p<0.01, ***p<0.001.