ArticleBritish journal of pharmacology2012
Thiazolidinedione-dependent activation of sphingosine kinase 1 causes an anti-fibrotic effect in renal mesangial cells.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Effect of FTY720P on lipid accumulation in HEPG2 cells.Scientific reports · 2023Article
- Therapeutic Implications of Ferroptosis in Renal Fibrosis.Frontiers in molecular biosciences · 2022Review
- Resveratrol Inhibits Lipopolysaccharide-Induced Extracellular Matrix Accumulation and Inflammation in Rat Glomerular Mesangial Cells by SphK1/S1P2/NF-κB Pathway.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Novel Insights into the Role of HDL-Associated Sphingosine-1-Phosphate in Cardiometabolic Diseases.International journal of molecular sciences · 2019Review
- Sphingosine Kinase 2 Deficiency Attenuates Kidney FibrosisJournal of the American Society of Nephrology : JASN · 2017Article
- Normalisation of surfactant protein -A and -B expression in the lungs of low birth weight lambs by 21 days old.PloS one · 2017Article
- Quantitative PPARγ expression affects the balance between tolerance and immunity.Scientific reports · 2016Article
- Sphingosine 1-phosphate is a ligand for peroxisome proliferator-activated receptor-γ that regulates neoangiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposePPARγ agonists [thiazolidinediones (TZDs)] are known to exert anti-fibrotic effects in the kidney. In addition, we previously demonstrated that sphingosine kinase 1 (SK-1) and intracellular sphingosine-1-phosphate (S1P), by reducing the expression of connective tissue growth factor (CTGF), have a protective role in the fibrotic process. EXPERIMENTAL APPROACH: Here, we investigated the effect of TZDs on intracellular sphingolipid levels and the transcriptional regulation of SK-1 in mesangial cells to evaluate potential novel aspects of the anti-fibrotic capacity of TZDs. KEY
resultsStimulation with the TZDs, troglitazone and rosiglitazone, led to increased S1P levels in rat mesangial cells. This was paralleled by increased SK-1 activity as a consequence of direct effects of the TZDs on SK-1 expression. GW-9662, a PPARγ antagonist, inhibited the stimulating effect of TZDs on SK-1 mRNA and activity levels and intracellular S1P concentrations. Furthermore, SK-1 up-regulation by TZDs was functionally coupled with lower amounts of pro-fibrotic CTGF. SK-1 inhibition with SKI II almost completely abolished this effect in a dose-dependent manner. Moreover, the CTGF lowering effect of TZDs was fully blocked in MC isolated from SK-1 deficient mice (SK-1(-/-) ) as well as in glomeruli of SK-1(-/-) mice compared with wild-type mice treated with TRO and RSG. CONCLUSION AND IMPLICATIONS: These data show that TZD-induced SK-1 up-regulation results in lower amounts of CTGF, demonstrating novel facets for the anti-fibrotic effects of this class of drugs.
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