ArticleBMC research notes2012
Phosphodiesterase inhibition mediates matrix metalloproteinase activity and the level of collagen degradation fragments in a liver fibrosis ex vivo rat model.
Article in BMC research notes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 25 citations in OpenAlex.
- The Role of RECK in Hepatobiliary Neoplasia Reveals Its Therapeutic Potential in NASH.Frontiers in endocrinology · 2021Review
- Molecular characterization of a precision-cut rat liver slice model for the evaluation of antifibrotic compounds.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- Tissue turnover of collagen type I, III and elastin is elevated in the PCLS model of IPF and can be restored back to vehicle levels using a phosphodiesterase inhibitor.Respiratory research · 2016Article
- Precision-Cut Kidney Slices as a Tool to Understand the Dynamics of Extracellular Matrix Remodeling in Renal Fibrosis.Biomarker insights · 2016Article
- Pathological Roles of Interleukin-22 in the Development of Recurrent Hepatitis C after Liver Transplantation.PloS one · 2016Article
- MicroRNA-34a Promotes Hepatic Stellate Cell Activation via Targeting ACSL1.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Novel insights into the function and dynamics of extracellular matrix in liver fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulation of extracellular matrix (ECM) and increased matrix metalloproteinase (MMP) activity are hallmarks of liver fibrosis. The aim of the present study was to develop a model of liver fibrosis combining ex vivo tissue culture of livers from CCl(4) treated animals with an ELISA detecting a fragment of type III collagen generated in vitro by MMP-9 (C3M), known to be associated with liver fibrosis and to investigate cAMP modulation of MMP activity and liver tissue turnover in this model.
findingsIn vivo: Rats were treated for 8 weeks with CCl(4)/Intralipid. Liver slices were cultured for 48 hours. Levels of C3M were determined in the supernatants of slices cultured without treatment, treated with GM6001 (positive control) or treated with IBMX (phosphodiesterase inhibitor). Enzymatic activity of MMP-2 and MMP-9 were studied by gelatin zymography. Ex vivo: The levels of serum C3M increased 77% in the CCl(4)-treated rats at week 8 (p < 0.01); Levels of C3M increased significantly by 100% in fibrotic liver slices compared to controls after 48 hrs (p < 0.01). By adding GM6001 or IBMX to the media, C3M was restored to control levels. Gelatin zymography demonstrated CCl(4)-treated animals had highly increased MMP-9, but not MMP-2 activity, compared to slices derived from control animals.
conclusionsWe have combined an ex vivo model of liver fibrosis with measurement of a biochemical marker of collagen degradation in the condition medium. This technology may be used to evaluate the molecular process leading to structural fibrotic changes, as collagen species are the predominant structural part of fibrosis. These data suggest that modulation of cAMP may play a role in regulation of collagen degradation associated with liver fibrosis.
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