ArticlePloS one2010
Differential regulation of the PGC family of genes in a mouse model of Staphylococcus aureus sepsis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- The miRNA Mirage: How Close Are We to Finding a Non-Invasive Diagnostic Biomarker in Endometriosis? A Systematic Review.International journal of molecular sciences · 2018Pooled it
- The involvement of regulatory non-coding RNAs in sepsis: a systematic review.Critical care (London, England) · 2016Pooled it
- Fiber-Dependent Microbiome Glycine Lipids Ameliorate Steatotic Liver Disease in Mice via Mitochondrial Enhancement.Gastro hep advances · 2026Article
- Mitochondria in innate immunity signaling and its therapeutic implications in autoimmune diseases.Frontiers in immunology · 2023Review
- Angiotensin II-mediated improvement of renal mitochondrial function via the AMPK/PGC-1α/NRF-2 pathway is superior to norepinephrine in a rat model of septic shock associated with acute renal injury.Annals of translational medicine · 2021Article
- Autophagy and Mitochondrial Homeostasis During Infection: A Double-Edged Sword.Frontiers in cell and developmental biology · 2021Review
- Mitochondrial Functions in Infection and Immunity.Trends in cell biology · 2020Review
- Mitochondrial Regulation of Macrophage Response Against Pathogens.Frontiers in immunology · 2020Review
- Midgut Mitochondrial Function as a Gatekeeper for Malaria Parasite Infection and Development in the Mosquito Host.Frontiers in cellular and infection microbiology · 2020Review
- Uncoupling Protein 2 Increases Blood Pressure in DJ -1 Knockout Mice.Journal of the American Heart Association · 2019Article
- Mitochondria in innate immune signaling.Translational research : the journal of laboratory and clinical medicine · 2018Review
- An innovative approach to predict immune-associated genes mutually targeted by cow and human milk microRNAs expression profiles.Veterinary world · 2018Article
- Exposure of Monocytic Cells to Lipopolysaccharide Induces Coordinated Endotoxin Tolerance, Mitochondrial Biogenesis, Mitophagy, and Antioxidant Defenses.Frontiers in immunology · 2018Article
- Role of microRNAs in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Review
- Differentially expressed miRNAs in sepsis-induced acute kidney injury target oxidative stress and mitochondrial dysfunction pathways.PloS one · 2017Article
- Mitofusin 2 Promotes Apoptosis of CD4Mediators of inflammation · 2017Article
- Mitochondrial dysfunction in inherited renal disease and acute kidney injury.Nature reviews. Nephrology · 2016Review
- Mitochondrial Quality Control as a Therapeutic Target.Pharmacological reviews · 2016Review
- Regulation of mitochondrial biogenesis and its intersection with inflammatory responses.Antioxidants & redox signaling · 2015Review
- Suppression of mitochondrial biogenesis through toll-like receptor 4-dependent mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling in endotoxin-induced acute kidney injury.The Journal of pharmacology and experimental therapeutics · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The PGC family of transcriptional co-activators (PGC-1alpha [Ppargc1a], PGC-1beta [Ppargc1b], and PRC [Pprc]) coordinates the upregulation of mitochondrial biogenesis, and Ppargc1a is known to be activated in response to mitochondrial damage in sepsis. Therefore, we postulated that the PGC family is regulated by the innate immune system. We investigated whether mitochondrial biogenesis and PGC gene expression are disrupted in an established model of Staphylococcus aureus sepsis both in mice with impaired innate immune function (TLR2-/- and TLR4-/-) and in wild-type controls. We found an early up-regulation of Ppargc1a and Ppargc1b post-infection (at 6 h) in WT mice, but the expression of both genes was concordantly dysregulated in TLR2-/- mice (no increase at 6 h) and in TLR4-/- mice (amplified at 6 h). However, the third family member, PRC, was regulated differently, and its expression increased significantly at 24 h in all three mouse strains (WT, TLR2-/-, and TLR4-/-). In silico analyses showed that Ppargc1a and Ppargc1b share binding sites for microRNA mmu-mir-202-3p. Thus, miRNA-mediated post-transcriptional mRNA degradation could account for the failure to increase the expression of both genes in TLR2-/- mice. The expression of mmu-mir-202-3p was measured by real-time PCR and found to be significantly increased in TLR2-/- but not in WT or TLR4-/- mice. In addition, it was found that mir-202-3p functionally decreases Ppargc1a mRNA in vitro. Thus, both innate immune signaling through the TLRs and mir-202-3p-mediated mRNA degradation are implicated in the co-regulation of Ppargc1a and Ppargc1b during inflammation. Moreover, the identification of mir-202-3p as a potential factor for Ppargc1a and Ppargc1b repression in acute inflammation may open new avenues for mitochondrial research and, potentially, therapy.
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