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. 2016 Sep 7;6:32771. doi: 10.1038/srep32771

Figure 9. Role of AMPK α2 in the fibrous dysplasia (FD) phenotype.

Figure 9

Two in vitro cell models were established that mimic the pathological features of FD: in one model, human BMSCs stably expressed a mutant GNAS protein harboring an R201H mutation (GsαR201H); in the second model, human BMSCs were treated with an excess of membrane-permeable cAMP. Osteogenic differentiation was induced in the cells. On days 0, 2, 4, and 7, the expression of the AMPK α2 subunit was evaluated by qRT-PCR (A–C). Results are expressed as fold change in mRNA abundance relative to day 0 cultures. AMPK α2 subunit was overexpressed in cells with and without cAMP treatment. These cells were induced to osteogenesis. The mRNA expression of ALP (D), IBSP (E), and OCN (F) was evaluated by qRT-PCR. Data are shown as mean ± SD. *P < 0.05, **P < 0.01.