Fig. 6: RORα mediates cholesterol-induced PD pathogenesis.
From: Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss
a Transcript levels of oxysterol-binding nuclear receptors in human GFs treated with IL1β (5 ng ml−1), TNFα (100 ng ml−1), cholesterol (200 μM), or 25-HC (20 μM) for 24 h (n = 3). b RORα transcriptional activity in human GFs treated with IL1β (2 ng ml−1), TNFα (50 ng ml−1), cholesterol (100 μM), and 25-HC (20 μM) for 24 h or infected with Ad-CH25H (800 MOI; n = 4). Representative RORα immunostaining images of the gingiva of human patients with PD (c) and ligature-induced PD mice (d). Scale bar, 25 μm. mRNA (e) and protein (f) levels in human GFs infected with Ad-RORα for 48 h (n ≥ 3). Representative RORα immunostaining (g), μCT, and H&E staining images (h) in mouse gingiva injected with an empty virus (Ad-C) or Ad-Rorα (1 × 109 PFU per 8 μl). Scale bar, 100 μm (left). Scale bar, 25 μm (right) (g). Scale bar, 100 μm (h). i Analysis of BMD and the CEJ-ABC distance in mouse maxillae injected intragingivally with Ad-C or Ad-Rorα (1 × 109 PFU per 8 μl; n = 10). n indicates the number of biologically independent samples and mice per group. Values are presented as the mean ± SEM based on a two-tailed t-test (i) and one-way ANOVA with Tukey’s test (a, b, e). (*P < 0.05, **P < 0.01, ***P < 0.001).
