Role of PPARα and HNF4α in Stress-Mediated Alterations in Lipid Homeostasis
Figure 2
In vitro evaluation of the role of glucocorticoids and hepatic adrenergic receptor-linked pathways in PPARα and target gene expression.
α. Following treatment of primary hepatocyte cultures with adrenergic receptor agonists for 24 hours, Acox, Cyp4a10, Cyp4a14, Acot1, Acot4, Lipin1 and Lipin2 mRNA levels were analyzed by qPCR. B. Ppara mRNA levels were also determined by qPCR in primary hepatocytes treated with either corticosterone, epinephrine or AR-agonists for 24 hours. Primary hepatocytes were also treated with AR-agonists in combination with the JNK inhibitor, SP600125 (SP), or the PKA inhibitors, H89 or sodium orthovanadate (NaOV). Values were quantified using the comparative CT methods normalized to β-actin and are expressed as mean ± SE (n = 3–4). Experiments were repeated three times. Comparisons were between control (DMSO) and drug-treated hepatocytes. C: control, CORT: corticosterone, PH: phenylephrine (alpha1-AR agonist), ISOP: isoprenaline (beta-AR agonist), EPIN: epinephrine (alpha- and beta-AR agonist), cAMP: 8-Br-cAMP. Group differences were calculated by one-way ANOVA, followed by Bonferonni's test. * P<0.025, **P<0.01, ***P<0.001.