ArticleWorld journal of gastroenterology2011
YKL-40 expression in CD14⁺ liver cells in acute and chronic injury.
Article in World journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Role of chitinase-3-like protein 1 in liver diseases: A comprehensive review.Genes & diseases · 2025Review
- Inflammatory Effects and Regulatory Mechanisms of Chitinase-3-like-1 in Multiple Human Body Systems: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Inhibition of Chitinase-3-like Protein 1 Reduced Epithelial-Mesenchymal Transition and Vascular Epithelial Cadherin Expression in Oesophageal Squamous Cell Carcinoma.Iranian journal of biotechnology · 2024Article
- Review
- Location-based prediction model for Crohn's disease regarding a novel serological marker, anti-chitinase 3-like 1 autoantibodies.World journal of gastroenterology · 2023Article
- CHI3L1 promotes myocardial fibrosis via regulating lncRNA TUG1/miR-495-3p/ETS1 axis.Apoptosis : an international journal on programmed cell death · 2023Article
- Chitinase-Like Protein Ym2 (Chil4) Regulates Regeneration of the Olfactory Epithelium via Interaction with Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Mesenchymal stem cells alleviate experimental immune-mediated liver injury via chitinase 3-like protein 1-mediated T cell suppression.Cell death & disease · 2021Article
- Chitinase 3-like-1 promotes intrahepatic activation of coagulation through induction of tissue factor in mice.Hepatology (Baltimore, Md.) · 2018Article
- The Effects of Ferulic Acid Against Oxidative Stress and Inflammation in Formaldehyde-Induced Hepatotoxicity.Inflammation · 2016Article
- Serum Markers of Epithelial Mesenchymal Transition as Predictors of HCV-induced Liver Fibrosis, Cirrhosis and Hepatocellular Carcinoma.Electronic physician · 2015Article
- The significance of YKL-40 protein in liver fibrosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Review
- Protective role of bortezomib in steatotic liver ischemia/reperfusion injury through abrogation of MMP activation and YKL-40 expression.Transplant immunology · 2014Article
- YKL-40 acts as an angiogenic factor to promote tumor angiogenesis.Frontiers in physiology · 2013Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo demonstrate that CD14⁺ cells are an important source of the growth factor YKL-40 in acute and chronic liver damage.
methodsRats were inoculated with one dose of CCl(4) to induce acute damage. Liver biopsies were obtained at 0, 6, 12, 24, 48 and 72 h. For chronic damage, CCl(4) was administered three days per week for 6 or 8 wk. Tissue samples were collected, and cellular populations were isolated by liver digestion and purified by cell sorting. YKL-40 mRNA and protein expression were evaluated by real-time polymerase chain reaction and western blot.
resultsAcute liver damage induced a rapid increase of YKL-40 mRNA beginning at 12 h. Expression peaked at 24 h, with a 26-fold increase over basal levels. By 72 h however, YKL-40 expression levels had nearly returned to control levels. On the other hand, chronic damage induced a sustained increase in YKL-40 expression, with 7- and 9-fold higher levels at 6 and 8 wk, respectively. The pattern of YKL-40 expression in different subpopulations showed that CD14⁺ cells, which include Kupffer cells, are a source of YKL-40 after acute damage at 72 h [0.09 relative expression units (REU)] as well as after chronic injury at 6 wk (0.11 REU). Hepatocytes, in turn, accounted for 0.06 and 0.01 REU after 72 h (acute) or 6 wk (chronic), respectively. The rest of the CD14⁻ cells (including T lymphocytes, B lymphocytes, natural killer and natural killer T cells) yielded 0.07 and 0.15 REU at 72 h and 6 wk, respectively. YKL-40 protein expression in liver was detected at 72 h as well as 6 and 8 wk, with the highest expression relative to controls (11-fold; P ≤ 0.05) seen at 6 wk. Macrophages were stimulated by lipopolysaccharide. We demonstrate that under these conditions, these cells showed maximum expression of YKL-40 at 12 h, with P < 0.05 compared with controls.
conclusionHepatic CD14⁺ cells are an YKL-40 mRNA and protein source in acute and chronic liver injury, with expression patterns similar to growth factors implicated in inflammation-fibrogenesis.
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