Fig. 5: Inhibition of PGC1A reduces triglyceride biosynthesis while promoting cholesterol esterification and biosynthesis, affects fatty acid uptake, and decreases cholesterol efflux in the RPE.

A qPCR analysis of mRNA levels of DGAT1, DGAT2, SOAT1, SOAT2, FATP2, FABP4, and CD36 (n = 3). B, C Protein levels of DGAT1, DGAT2, SOAT1 and SOAT2 (n = 3). D, E Protein levels of FATP2, FABP4, and CD36 (n = 3). F, G PGC1A inhibition significantly reduced protein levels of low-density lipoprotein receptor (LDLR) and cholesterol efflux-related proteins, ABCA1, ABCG1, and ABCG5 (n = 3). H–K Inhibition of PGC1A significantly decreased phosphorylation of HMGCR at Ser872 and reduced phosphorylation of AMPKα at Thr172 (n = 3). GAPDH was used for internal control and statistical normalization (n = 3). ImageJ was used for densitometry analysis. Unpaired t-test was performed for statistical analysis. Graph represents mean ± SEM, *P ≤ 0.05, **P ≤ 0.01, *** P ≤ 0.001, n.s. means no significance.