ArticleThe Journal of infectious diseases2013
Suppression of PTRF alleviates the polymicrobial sepsis induced by cecal ligation and puncture in mice.
Article in The Journal of infectious diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- A ZDHHC3-USP5-PTRF axis links palmitoylation to ferroptosis-associated phenotypes in melanoma.Cell death & disease · 2026Article
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- Caveolae and the oxidative stress response.Biochemical Society transactions · 2023Article
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- Non-alcoholic fatty liver disease combined with rheumatoid arthritis exacerbates liver fibrosis by stimulating co-localization of PTRF and TLR4 in rats.Frontiers in pharmacology · 2023Article
- Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
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- Suppression of PTRF Alleviates Post-Infectious Irritable Bowel Syndrome via Downregulation of the TLR4 Pathway in Rats.Frontiers in pharmacology · 2021Article
- Immune response and differentially expressed proteins in the lung tissue of BALB/c mice challenged by aerosolized Brucella melitensis 5.The Journal of international medical research · 2018Article
- miR-15a/16 regulates macrophage phagocytosis after bacterial infection.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundSepsis and sepsis-associated organ failure are devastating conditions. Understanding the detailed cellular/molecular mechanisms involved in sepsis should lead to the identification of novel therapeutic targets.
methodsCecal ligation and puncture (CLP) was used as a polymicrobial sepsis model in vivo to determine mortality and end-organ damage. Macrophages were adopted as the cellular model in vitro for mechanistic studies.
resultsPTRF+/- mice survived longer and suffered less organ damage after CLP. Reductions in nitric oxide (NO) and iNOS biosynthesis were observed in plasma, macrophages, and vital organs in the PTRF+/- mice. Using an acute sepsis model after CLP, we found that iNOS-/- mice had a comparable level of survival as the PTRF+/- mice. Similarly, polymerase I transcript release factor (PTRF) deficiency resulted in decreased iNOS and NO/ROS production in macrophages in vitro. Mechanistically, lipopolysaccharide (LPS) enhanced the co-localization and interaction between PTRF and TLR4 in lipid rafts. Deletion of PTRF blocked formation of the TLR4/Myd88 complex after LPS. Consistent with this, lack of PTRF impaired the TLR4 signaling, as shown by the decreased p-JNK, p-ERK, and p-p38, which are upstream factors involved in iNOS transcription.
conclusionPTRF is a crucial regulator of TLR4 signaling in the development of sepsis.
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Registered trials
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