ArticleEBioMedicine2017
p32 is Required for Appropriate Interleukin-6 Production Upon LPS Stimulation and Protects Mice from Endotoxin Shock.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
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- An N-terminal and ankyrin repeat domain interactome of Shank3 identifies the protein complex with the splicing regulator Nono in mice.Genes to cells : devoted to molecular & cellular mechanisms · 2024Article
- Cardiomyocyte-specific deletion of the mitochondrial transporter Abcb10 causes cardiac dysfunction via lysosomal-mediated ferroptosis.Bioscience reports · 2024Article
- Improving lysosomal ferroptosis with NMN administration protects against heart failure.Life science alliance · 2023Article
- Inflammatory macrophages reprogram to immunosuppression by reducing mitochondrial translation.Nature communications · 2023Article
- Cancer genomic profiling identified dihydropyrimidine dehydrogenase deficiency in bladder cancer promotes sensitivity to gemcitabine.Scientific reports · 2022Article
- The regulation of T helper cell polarization by the diterpenoid fraction ofFrontiers in pharmacology · 2022Article
- Metabolic analysis of mouse bone-marrow-derived dendritic cells using an extracellular flux analyzer.STAR protocols · 2021Article
- Attenuating Effect ofFrontiers in nutrition · 2021Article
- Mitochondrial Reactive Oxygen Species Are Essential for the Development of Psoriatic Inflammation.Frontiers in immunology · 2021Article
- Article
- Analysis of Polymorphisms in the Mediator Complex Subunit 13-like (Med13L) Gene in the Context of Immune Function and Development of Experimental Arthritis.Archivum immunologiae et therapiae experimentalis · 2018Article
- ATF4 Involvement in TLR4 and LOX-1-Induced Host Inflammatory Response toJournal of ophthalmology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a major cause of morbidity and mortality in seriously ill patients and mitochondrial dysfunction is associated with poor outcomes in septic patients. Although interleukin-6 (IL-6) is a good prognostic marker for sepsis, the relationship between mitochondrial dysfunction and IL-6 remains poorly understood. We identified p32/C1QBP/HABP1 as a regulator of IL-6 production in response to lipopolysaccharide (LPS). LPS induced IL-6 overproduction in p32 deficient mouse embryonic fibroblasts (MEFs) through NF-κB independent but activating transcription factor (ATF) 4 dependent pathways. Short hairpin RNA-based knockdown of ATF4 in p32 deficient MEFs markedly inhibited LPS-induced IL-6 production. Furthermore, MEFs treated with chloramphenicol, an inhibitor of mitochondrial translation, produced excessive IL-6 via ATF4 pathways. Using a LPS-induced endotoxin shock model, mice with p32 ablation in myeloid cells showed increased lethality and overproduction of IL-6. Thus, this study provides a molecular link how mitochondrial dysfunction leads to IL-6 overproduction and poor prognosis of sepsis.
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