Fig. 2: Neuronal transcriptional response to AdipoRon extends beyond metabolic regulation.
From: Reversal of neuronal tau pathology via adiponectin receptor activation
A Pathway enrichment was determined via GSEA of tau neuron AR-responsive KEGG pathways using RNA-seq data (n = 5–6 pups per genotype per treatment). B As above for AR-responsive KEGG pathways in WT neurons. C STRING analysis and heatmap displaying log2FC of Neuroactive Ligand Receptor Interaction Pathway genes sub-grouped via Markov Cluster Algorithm (clusters ≥ 4 genes shown) in Tau neurons in response to AR. D Heatmap of lysosome pathway detected by GSEA in AR-treated Tau and WT neurons compared to untreated WT. E, F Immunofluorescent detection and quantification of autophagosome markers LC3b (n = 4–6 mice, n = 33–56 neurons per treatment) and p62 (n = 3 mice, n = 29–43 neurons per treatment) in Tau neurons after 24-h treatment with 10 μM AdipoRon ± 8 μM Compound C. G Western blot of LAMP2A and LC3 with representative ponceau in neurons after 24-h treatment with 10 μM AdipoRon (LAMP2A: n = 6 mice per treatment; LC3: n = 9 mice per treatment). Significance determined by one-way ANOVA with Tukey’s multiple comparison’s test or Student’s t test. Data shown as mean ± SEM *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
