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Fig. 5 | Fluids and Barriers of the CNS

Fig. 5

From: Fasting upregulates the monocarboxylate transporter MCT1 at the rat blood-brain barrier through PPAR δ activation

Fig. 5

Effect of PPAR activation in primary cultured rat CECs. (a-c) qRT-PCR analysis of Angptl4 and Cpt1a gene expression. (a,b) Cells were treated as indicated with synthetic agonists selective for PPAR α (fenofibrate, feno), PPAR δ (GW501516, GW0742), or PPAR γ (rosiglitazone, rosi) and synthetic antagonists selective for PPAR α (GW6471) or PPAR δ (GSK0660). (c) Cells were treated as indicated with palmitate (PALM) or oleate (OLE) in the presence of L-carnitine (carn). (a-c) Data are presented as fold increase to the control. Mean ± SD. One-way ANOVA with Holm-Sidak’s multiple comparisons test. (d) Non-targeted quantitative proteomics of CECs treated for 48 h with 100 nM GW0742 ± 2 µM GSK0660 or left untreated (Control) (n = 3). Heatmap of the standard deviations from mean protein intensities for the 60 proteins simultaneously upregulated in GW0742 vs. Control and downregulated in GW0742 + GSK0660 vs. GW0742 (p value ≤ 0.05). Note that MOT1 is the official name of MCT1 in the UniProt database. (e) KEGG enriched pathways in the proteins shown in d. (a-e) Culture medium contained 0.38% BSA in all conditions including control

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