Combined transcriptomics and proteomics analysis unveiled the impact of vitamin C in modulating specific mitochondrial protein abundance in the mouse liver.
Ontology highlight
ABSTRACT: Vitamin C (ascorbate) is a crucial antioxidant and an essential cofactor of biosynthetic and regulatory enzymes. Unlike humans, mice can synthesize vitamin C thanks to the key enzyme gulonolactone oxidase (Gulo). In the present study, we used the Gulo-/- mouse model, which cannot synthesize their own ascorbate to determine the impact of this vitamin on both the transcriptomics and proteomics profiles in the liver. The study included Gulo-/- mouse groups treated with either sub-optimal or optimal vitamin C concentrations in drinking water. We found a distinctive difference in the mRNA and protein profiles as a function of sex between all the mouse groups. Despite this sexual dimorphism, Spearman correlation analyses were conducted to divulge which transcripts and proteins correlated with hepatic vitamin C concentrations in both females and males. Such analysis on transcriptomics data from females and males revealed changes in a wide array of biological processes involved in glucose, lipid, steroid, and glutathione metabolisms as well as in acute-phase response. Furthermore, although several proteins of the mitochondrial complex III significantly correlated with vitamin C concentrations, their corresponding transcripts did not correlate with vitamin C in both females and males. Thus, this side-by-side comparison between transcriptome and proteome supported the view that post-transcriptional processes play a major role in the regulation of cellular respiration in the liver upon vitamin C deficiency. Our findings suggest that transcriptome profiling alone provides an incomplete picture of molecular changes associated with vitamin C deficiency in the liver of mice and examination of changes in protein abundances is essential to unveil variations that are not transcriptionally regulated.
ORGANISM(S): Mus musculus
PROVIDER: GSE233598 | GEO | 2023/06/01
REPOSITORIES: GEO
ACCESS DATA