{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cherry AD"],"funding":["BLRD VA","NIAID NIH HHS","NHLBI NIH HHS","PHS HHS"],"pagination":["41-52"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3879563"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["289(1)"],"pubmed_abstract":["A key transcriptional regulator of cell metabolism, the peroxisome proliferator-activated receptor γ co-activator 1-α (PPARGC-1-α or PGC-1α), also regulates mitochondrial biogenesis, but its role in antioxidant gene regulation is not well understood. Here, we asked whether genetic heterozygosity of PGC-1α modulates gene expression for the mitochondrial antioxidant enzyme SOD-2 during hepatic inflammatory stress. Using Staphylococcus aureus peritonitis in mice, we found significant Sod2 gene induction in WT mice, whereas PGC-1α heterozygotes (PGC-1α(+/-)) failed to augment Sod2 mRNA and protein levels. Impaired Sod2 regulation in PGC-1α(+/-) mice was accompanied by oxidative stress shown by elevated mitochondrial GSSG/GSH and protein carbonyls. In silico analysis of the mouse proximal Sod2 "],"journal":["The Journal of biological chemistry"],"pubmed_title":["Peroxisome proliferator-activated receptor γ co-activator 1-α as a critical co-activator of the murine hepatic oxidative stress response and mitochondrial biogenesis in Staphylococcus aureus sepsis."],"pmcid":["PMC3879563"],"funding_grant_id":["R01 AI095424","I01 BX001926","R01-A1095424","R01-HL108801","P01 HL108801"],"pubmed_authors":["Suliman HB","Cherry AD","Bartz RR","Piantadosi CA"],"additional_accession":[]},"is_claimable":false,"name":"Peroxisome proliferator-activated receptor γ co-activator 1-α as a critical co-activator of the murine hepatic oxidative stress response and mitochondrial biogenesis in Staphylococcus aureus sepsis.","description":"A key transcriptional regulator of cell metabolism, the peroxisome proliferator-activated receptor γ co-activator 1-α (PPARGC-1-α or PGC-1α), also regulates mitochondrial biogenesis, but its role in antioxidant gene regulation is not well understood. Here, we asked whether genetic heterozygosity of PGC-1α modulates gene expression for the mitochondrial antioxidant enzyme SOD-2 during hepatic inflammatory stress. Using Staphylococcus aureus peritonitis in mice, we found significant Sod2 gene induction in WT mice, whereas PGC-1α heterozygotes (PGC-1α(+/-)) failed to augment Sod2 mRNA and protein levels. Impaired Sod2 regulation in PGC-1α(+/-) mice was accompanied by oxidative stress shown by elevated mitochondrial GSSG/GSH and protein carbonyls. In silico analysis of the mouse proximal Sod2 ","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jan","modification":"2025-04-26T06:16:55.525Z","creation":"2019-03-27T01:19:20Z"},"accession":"S-EPMC3879563","cross_references":{"pubmed":["24253037"],"doi":["10.1074/jbc.M113.512483","10.1074/jbc.m113.512483"]}}