Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.
Skip to main content
Fig. 6 | Cellular & Molecular Biology Letters

Fig. 6

From: Maternal high-fat diet orchestrates offspring hepatic cholesterol metabolism via MEF2A hypermethylation-mediated CYP7A1 suppression

Fig. 6

Maternal high-fat diet feeding induces hepatic mef2a hypermethylation in offspring. A CpG sites measured in Mef2a promoter. B DNA methylation levels of different CpG sites in Mef2a promoter. C Average DNA methylation level in Mef2a promoter. D Correlation between Mef2a methylation level and Mef2a mRNA expression. E Correlation between Mef2a methylation level and MEF2A protein expression. F mRNA expression of Mef2a in 5-AZA-treated HepG2 cells. G Representative immunoblot images for MEF2A in 5-AZA-treated HepG2 cells. H Immunoblot analysis of MEF2A in 5-AZA-treated HepG2cells. I Relative luciferase activity of methylated or unmethylated plasmids in H9C2 cells. F1, the second generation (offspring); Ctrl, standard diet; HFD, high-fat diet; MEF2A, myocyte enhancer factor 2A; 5-AZA, 5-azacitidine. Data presented as the mean ± SEM. *P < 0.05, ***P < 0.001 versus F1-Ctrl group. n = 7–8 litters/group, one male offspring per litter. *P < 0.05, ***P < 0.001 versus Ctrl. n = 6–7 litters for F1-Ctrl group, n = 6–7 litters for F1-HFD group, one male offspring per litter

Back to article page

Cellular & Molecular Biology Letters

ISSN: 1689-1392

Contact us