Fig. 4. PKA signaling is activated by an increase in PKA Cα in HIF2α deficient adipocytes.
a Heatmap of upregulated DEGs in iWAT of HIF2α AKO mice upon cold exposure (3 days). b KEGG pathway and GO cellular component enrichment analysis upon cold exposure (3 days). c Scatter plot of thermogenesis-related DEGs upon cold exposure (3 days). d DEGs interaction network in iWAT of HIF2α AKO mice upon cold exposure (3 days). e mRNA levels in iWAT from WT (n = 7), HIF1α AKO (n = 6), HIF2α AKO (n = 6), and HIF1/2α DKO (n = 6) mice upon cold exposure (3 days). f, g Western blot analysis of PKA Cα in iWAT from WT and HIF2α AKO mice upon f cold exposure (3 days) or g daily CL administration (0.5 mg/kg, 4 days). h Western blot analysis of PKA signaling and UCP1 in iWAT from WT and HIF2α AKO mice upon TN or cold exposure (6 h). i Western blot analysis of PKA signaling in iWAT from WT and HIF2α AKO mice upon CL administration (0.5 mg/kg, 4 h). j Western blot analysis of PKA signaling and UCP1 in beige adipocytes from WT and HIF2α AKO mice without or with ISO (5 μM, 1 h). k Glycerol concentration in culture media of beige adipocytes from WT (n = 5) and HIF2α AKO (n = 5) mice without or with ISO (5 μM, 3 h). l Intracellular cAMP levels of beige adipocytes from WT (n = 4) and HIF2α AKO (n = 4) mice without or with ISO (1 μM, 15 min). m mRNA levels in beige adipocytes from WT (n = 3) and HIF2α AKO (n = 3) mice. n Western blot analysis of PKA Cα in beige adipocytes from WT and HIF2α AKO mice. o mRNA levels in beige adipocytes infected with Admock (n = 4) or AdHIF2α (n = 4). p Western blot analysis of PKA Cα beige adipocytes infected with Admock or AdHIF2α. Data were expressed as the mean ± SEM by either two-tailed unpaired Student t-tests in (m, o), one-way ANOVA in (e), or two-way ANOVA in (k, l) followed by Holm–Sidak’s multiple comparisons test. ISO isoproterenol.