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. 2017 Jul 31;114(33):E6867–E6874. doi: 10.1073/pnas.1706915114

Fig. 5.

Fig. 5.

STAT1 is not a major mediator for the observed inhibitory effect of IFNG on cytokine-driven odontoblastic differentiation. (A) KD of STAT1 does not abolish the inhibitory effect of IFNG on OSM-induced DPSC differentiation measured by ALP activity. DPSCs were preinfected with lentiviruses of scrambled (sc) shRNA or STAT1 shRNA and subsequently transduced with lentiviruses containing control vector, IFNG, OSM, or IFNG plus OSM. After 6 d, ALP activity was measured. (B and C) Overexpression of STAT1 does not prevent OSM-induced DPSC differentiation as potently as IFNG. DPSCs were incubated with lentiviruses containing control vector, IFNG, STAT1, OSM, IFNG plus OSM, or STAT1 plus OSM, followed by ALP assay, ARS staining (B), or qPCR analysis to determine mRNA levels of ALP, RUNX2, and Collagen I (C). Data are shown as mean + SD (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001.