ArticlePloS one2012
Interference with oligomerization and glycosaminoglycan binding of the chemokine CCL5 improves experimental liver injury.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Metabolism of hepatic stellate cells in chronic liver diseases: emerging molecular and therapeutic interventions.Theranostics · 2025Review
- Article
- Fibroblast Growth Factor-21 ameliorates hepatic encephalopathy by activating the STAT3-SOCS3 pathway to inhibit activated hepatic stellate cells.EXCLI journal · 2020Article
- Anti-inflammatory properties of ursodeoxycholyl lysophosphatidylethanolamide in endotoxin-mediated inflammatory liver injury.PloS one · 2018Article
- Chemokines from a Structural Perspective.International journal of molecular sciences · 2017Review
- Glycosaminoglycan Interactions with Chemokines Add Complexity to a Complex System.Pharmaceuticals (Basel, Switzerland) · 2017Review
- Sympathetic Nervous System Control of Carbon Tetrachloride-Induced Oxidative Stress in Liver through α-Adrenergic Signaling.Oxidative medicine and cellular longevity · 2016Article
- RANTES/CCL5 mediated-biological effects depend on the syndecan-4/PKCα signaling pathway.Biology open · 2014Article
- Caveolin-1 regulates chemokine receptor 5-mediated contribution of bone marrow-derived cells to dermal fibrosis.Frontiers in pharmacology · 2014Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe chemokine CCL5 is involved in the recruitment of immune cells and a subsequent activation of hepatic stellate cells (HSC) after liver injury. We here investigate whether inhibition of CCL5 oligomerization and glycosaminoglycan binding by a mutated CCL5 protein ((44)AANA(47)-CCL5) has the potential to ameliorate liver cell injury and fibrosis in vivo. METHODOLOGY: Liver injury was induced in C57BL/6 mice by intraperitoneal injection of carbon tetrachloride (CCl(4)) in an acute and a chronic liver injury model. Simultaneously, mice received either (44)AANA(47)-CCL5 or vehicle. Liver cell necrosis and fibrosis was analyzed by histology, and measurement of serum transaminases and hydroxyproline. Intrahepatic mRNA expression of fibrosis and inflammation related genes were determined by quantitative RT-PCR and infiltration of immune cells was assessed by FACS analysis and immunocytochemistry. In vitro, HSC were stimulated with conditioned media of T-cell enriched splenocytes. PRINCIPAL
findings(44)AANA(47)-CCL5 treated mice displayed a significantly reduced degree of acute liver injury (liver cell necrosis, transaminases) and fibrosis (Sirus red positive area and hydroxyproline content) compared to vehicle treated mice. Ameliorated fibrosis by (44)AANA(47)-CCL5 was associated with a decreased expression of fibrosis related genes, decreased α-smoth muscle antigen (αSMA) and a reduction of infiltrating immune cells. In the acute model, (44)AANA(47)-CCL5 treated mice displayed a reduced immune cell infiltration and mRNA levels of TNF, IL-1 and CCL3 compared to vehicle treated mice. In vitro, conditioned medium of T-cell enriched splenocytes of (44)AANA(47)-CCL5 treated mice inhibited the chemotaxis and proliferation of HSC.
conclusionsThe results provide evidence that inhibition of oligomerization and glycosaminoglycan binding of the chemokine CCL5 is a new therapeutic strategy for the treatment of acute and chronic liver injuries and represents an alternative to chemokine receptor antagonism.
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