Mechanistic
and biological effects of the alternative site PPARγ
ligand 2. (a) 2 caused distinguished effects
on co-regulator recruitment by PPARγ with activating and inactivating
contributions. Pioglitazone (3 μM), 2 (30 μM),
GW9662 (10 μM). Data are the mean ± SD ΔHTRF vs DMSO; n = 4. (b) Pioglitazone (10 μM) and the RXR agonist
SR11237 (10 μM) increased and 2 (50 μM) diminished
heterodimerization of PPARγ with RXR. 2 also blocked
the dimer-stabilizing effects of pioglitazone and SR11237. Data are
the mean ± SD HTRF vs DMSO; n = 3. (c) In contrast
to pioglitazone, 2 induced no differentiation of human
adipocyte-derived stem cells (ASC). Data are the mean ± SD relative
Oil Red O (ORO) deposition compared to pioglitazone; n = 3. (d) Representative images of ASC differentiation experiments
stained with ORO. (e) Differential gene expression in HepG2 cells
treated with 2 (20 μM) versus DMSO (0.1%). Volcano
plot shows log2(fold change) in the gene expression level (x-axis) versus the statistical significance level (−log10(p-value); y-axis). (f) Compared effects
of 2 and GA on gene expression. Heat map shows induced
(blue), downregulated (red), and nonregulated (black) genes. (g–i)
Selected genes regulated by treatment with 2 (20 μM)
associated with FOXO signaling (g), adipo–/lipogenesis (h),
TOR signaling (i), cell cycle (i), apoptosis (i), and ATP generation
(i). Heat maps show log2(fold change) in the gene expression of significantly
(p-value <0.05) regulated genes. (j) Treatment
with 2 (20 μM, 16 h) enhanced the inactivating
phosphorylation of FOXO3a at Ser253. Data are the mean ± S.E.M.; n = 6. Western blots in the Supporting Information. (k)
Pioglitazone enhanced, 2 decreased FOXO activity in HepG2
cells over time. Data are the mean ± S.E.M. FHRE activity; n ≥ 3.