Figure 2. Exogenous PPARγ or H₂O₂ rescues adipocyte differentiation in the presence of mitochondrial targeted antioxidants.

(A) Human MSCs were infected with AdPPARγ2 or AdNull at day 1 and treated with TPP (500nM) or MitoCP (500nM) +/− 5 μM troglitazone (Tro) starting at day 2. Subsequently, at day 21 of differentiation cells were stained with Oil Red O and optical density (OD) values were assessed. N=3 ± SEM.

(B) Gene expression of PPARγ2 and its target genes at day 7 of differentiation in human MSCs infected with AdPPARγ2 or AdNull at day 1 and treated with TPP (500nM) or MitoCP (500nM) +/− 5 μM troglitazone (Tro.) starting at day 2. N=3 ± SEM.

(C) Western blot analysis of PPARγ protein at Day 5 of adipocyte differentiation. Human MSCs were infected with AdNull or AdPPARγ2 at day 1 and administered 500 nM of MitoCP or TPP control starting at day 2.

(D) Intracellular H₂O₂ levels of human MSCs treated with galactose (0.5mM) with or without galactose oxidase (GAO, 0.015U/ml) in the presence of 500 nM of TPP or MitoCP starting at Day 2. N=3 ± SEM.

(E) Human MSCs were treated with galactose (0.5mM) with or without GAO (0.015U/ml) plus 500 nM of TPP or MitoCP starting at day 2. Subsequently, at day 21 of differentiation cells were stained with Oil Red O and optical density (OD) values were assessed. N=3 ± SEM.

(F) Human MSCs were treated with galactose (0.5mM) with or without GAO (.015U/ml) plus 500 nM TPP or MitoCP starting at day 2. Gene expression was analyzed at day 7 of differentiation. N=3 ± SEM.