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. 2020 Aug 25;14(10):2533–2545. doi: 10.1002/1878-0261.12775

Fig. 4.

Fig. 4

Compounds that increase cAMP levels differentially modulate sterol metabolism. (A) LP1 cells were treated with 4 μm fluvastatin ± 5 μm dipyridamole, 20 μm cilostazol, 10 μm forskolin, or 0.1 mm db‐cAMP for 16 h, and RNA was isolated to assay for HMGCR, HMGCS1 and INSIG1 expression by qRT–PCR. mRNA expression data are normalized to GAPDH expression. Data are represented as the mean + SD. *P < 0.05 (one‐way ANOVA with Tukey's multiple comparisons test, where the indicated groups were compared to the solvent controls group), # P < 0.05 (one‐way ANOVA with Tukey's multiple comparisons test, comparing the two indicated groups). (B) LP1 cells were treated with 4 μm fluvastatin ± 5 μm dipyridamole, 20 μm cilostazol, 10 μm forskolin, or 0.1 mm db‐cAMP for 24 h, and protein was isolated to assay for HMGCR expression by immunoblotting. 1 = HMGCR oligomer, 2 = HMGCR monomer. Immunoblots are representative of three independent experiments. (C) LP1 cells were treated with 4 μm fluvastatin ± 5 μm dipyridamole or 20 μm cilostazol for 8 h, and protein was isolated to assay for SREBP2 cleavage (activation) by immunoblotting. F, full‐length SREBP2; C, cleaved SREBP2. Immunoblots are representative of three independent experiments.