Figure 1. LXRs signaling regulates cholesterol metabolism in nodose ganglia neurons.
(A) Regulation of selected target genes in nodose ganglia (NG) following liver X receptor (LXR) agonist treatment in vivo (left panel) n = 5–8 per group. **p < 0.005. (B) NG organotypic slices were prepared from LXRsNav or LXRsfl/fl treated with GW3965 (5 μM) or vehicle for 4 hr. Quantitative PCR (qPCR) data are expressed as average fold-change relative to vehicle ± S.E.M., n = 3 independent experiments. # and *indicates p < 0.5, **p < 0.005. (C) Quantification of total cholesterol. Values were expressed as ng of cholesterol per NG, n = 6. ## and **p < 0.001. (right panel). Neurons isolated from LXRsNav or control mice NG were subjected to Filipin staining (representative images of staining from 3 individual mice).
Figure 1—figure supplement 1. Ablation of LXR in the NAV1.8 positive neurons.
qPCR analysis detecting the expression of truncated isoforms of Nr1h3 (A) and Nr1h2 (B) in NG, liver, white adipose, brown adipose tissues (BATs), and muscle. Error bars show S.E.M. **indicates p < 0.01.