ArticleWorld journal of gastroenterology2006
Gene expression profiles of hepatic cell-type specific marker genes in progression of liver fibrosis.
Article in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
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- Bone marrow derived-mesenchymal stem cells downregulate IL17A dependent IL6/STAT3 signaling pathway in CCl4-induced rat liver fibrosis.PloS one · 2018Article
- Peroxisome Proliferator Activated Receptor Agonists Modulate Transposable Element Expression in Brain and Liver.Frontiers in molecular neuroscience · 2018Article
- Exemestane Attenuates Hepatic Fibrosis in Rats by Inhibiting Activation of Hepatic Stellate Cells and Promoting the Secretion of Interleukin 10.Journal of immunology research · 2017Article
- Inhibition of vascular endothelial growth factor signaling facilitates liver repair from acute ethanol-induced injury in zebrafish.Disease models & mechanisms · 2016Article
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- PPAR agonists regulate brain gene expression: relationship to their effects on ethanol consumption.Neuropharmacology · 2014Article
- Extracellular matrix and liver disease.Antioxidants & redox signaling · 2014Review
- Branched-chain amino acids inhibit the TGF-beta-induced down-regulation of taurine biosynthetic enzyme cysteine dioxygenase in HepG2 cells.Amino acids · 2014Article
- Sub-chronic toxicity study in rats orally exposed to nanostructured silica.Particle and fibre toxicology · 2014Article
- Exposure to cobalt causes transcriptomic and proteomic changes in two rat liver derived cell lines.PloS one · 2013Article
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- NDRG2 ameliorates hepatic fibrosis by inhibiting the TGF-β1/Smad pathway and altering the MMP2/TIMP2 ratio in rats.PloS one · 2011Article
- Daily genetic profiling indicates JAK/STAT signaling promotes early hepatic stellate cell transdifferentiation.World journal of gastroenterology · 2010Article
- Toxicogenomic biomarkers for liver toxicity.Journal of toxicologic pathology · 2009Article
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
aimTo determine the gene expression profile data for the whole liver during development of dimethylni-trosamine (DMN)-induced hepatic fibrosis.
methodsMarker genes were identified for different types of hepatic cells, including hepatic stellate cells (HSCs), Kupffer cells (including other inflammatory cells), and hepatocytes, using independent temporal DNA microarray data obtained from isolated hepatic cells.
resultsThe cell-type analysis of gene expression gave several key results and led to formation of three hypotheses: (1) changes in the expression of HSC-specific marker genes during fibrosis were similar to gene expression data in in vitro cultured HSCs, suggesting a major role of the self-activating characteristics of HSCs in formation of fibrosis; (2) expression of mast cell-specific marker genes reached a peak during liver fibrosis, suggesting a possible role of mast cells in formation of fibrosis; and (3) abnormal expression of hepatocyte-specific marker genes was found across several metabolic pathways during fibrosis, including sulfur-containing amino acid metabolism, fatty acid metabolism, and drug metabolism, suggesting a mechanistic relationship between these abnormalities and symptoms of liver fibrosis.
conclusionAnalysis of marker genes for specific hepatic cell types can identify the key aspects of fibrogenesis. Sequential activation of inflammatory cells and the self-supporting properties of HSCs play an important role in development of fibrosis.
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