ArticlePloS one2013
Comparative analysis of hepatic CD14 expression between two different endotoxin shock model mice: relation between hepatic injury and CD14 expression.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- The Pivotal Role of Presepsin in Assessing Sepsis-Induced Cholestasis.Diagnostics (Basel, Switzerland) · 2024Article
- Deletion of caveolin-1 attenuates LPS/GalN-induced acute liver injury in mice.Journal of cellular and molecular medicine · 2018Article
- Expression of glutathione S-transferase A1, a phase II drug-metabolizing enzyme in acute hepatic injury on mice.Experimental and therapeutic medicine · 2017Article
- Comparative proteomic analysis of the effects of high-concentrate diet on the hepatic metabolism and inflammatory response in lactating dairy goats.Journal of animal science and biotechnology · 2016Article
- Exogenous normal lymph reduces liver injury induced by lipopolysaccharides in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014Article
- Study of the effects of Escherichia coli lipopolysaccharide on innate immunity: The expression profile of TLR4 and CD14 genes in rat liver.Open veterinary journalArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD14 is a glycoprotein that recognizes gram-negative bacterial lipopolysaccharide (LPS) and exists in both membrane-bound and soluble forms. Infectious and/or inflammatory diseases induce CD14 expression, which may be involved in the pathology of endotoxin shock. We previously found that the expression of CD14 protein differs among the endotoxin shock models used, although the reasons for these differences are unclear. We hypothesized that the differences in CD14 expression might be due to liver injury, because the hepatic tissue produces CD14 protein. We investigated CD14 expression in the plasma and liver in the carrageenan (CAR)-primed and D-galN-primed mouse models of endotoxin shock. Our results showed that severe liver injury was not induced in CAR-primed endotoxin shock model mice. In this CAR-primed model, the higher mRNA and protein expression of CD14 was observed in the liver, especially in the interlobular bile duct in contrast to D-galN-primed-endotoxin shock model mice. Our findings indicated that the molecular mechanism(s) underlying septic shock in CAR-primed and D-galN-primed endotoxin shock models are quite different. Because CD14 expression is correlated with clinical observations, the CAR-primed endotoxin shock model might be useful for studying the functions of CD14 during septic shock in vivo.
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