ArticleBritish journal of pharmacology2011
Characterization of the mechanisms of the increase in PPARδ expression induced by digoxin in the heart using the H9c2 cell line.
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Roles of distinct nuclear receptors in diabetic cardiomyopathy.Frontiers in pharmacology · 2024Review
- PTX3 from vascular endothelial cells contributes to trastuzumab-induced cardiac complications.Cardiovascular research · 2023Article
- Live cell screening identifies glycosides as enhancers of cardiomyocyte cell cycle activity.Frontiers in cardiovascular medicine · 2022Article
- Etanercept Ameliorates Cardiac Fibrosis in Rats with Diet-Induced Obesity.Pharmaceuticals (Basel, Switzerland) · 2021Article
- TGR5 activation ameliorates hyperglycemia-induced cardiac hypertrophy in H9c2 cells.Scientific reports · 2019Article
- Ginsenoside Rh2 Improves Cardiac Fibrosis via PPARδ-STAT3 Signaling in Type 1-Like Diabetic Rats.International journal of molecular sciences · 2017Article
- Lanatoside C Promotes Foam Cell Formation and Atherosclerosis.Scientific reports · 2016Article
- Alpha1a-adrenoceptor genetic variant induces cardiomyoblast-to-fibroblast-like cell transition via distinct signaling pathways.Cellular signalling · 2014Article
- Merit of ginseng in the treatment of heart failure in type 1-like diabetic rats.BioMed research international · 2014Article
- Ginseng is useful to enhance cardiac contractility in animals.BioMed research international · 2014Article
- Cardiac peroxisome proliferator-activated receptor δ (PPARδ) as a new target for increased contractility without altering heart rate.PloS one · 2013Article
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6 authors.
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Abstract
background and purposeDigoxin has been used as an inotropic agent in heart failure for a long time. Troponin I (TnI) phosphorylation is related to cardiac contractility, and the genes are regulated by peroxisome proliferator-activated receptors (PPARs). Our previous studies indicated that cardiac abnormality related to the depressed expression of PPARδ in the hearts of STZ rats is reversed by digoxin. However, the cellular mechanisms for this effect of digoxin have not been elucidated. The aim of the present study was to investigate possible mechanisms for this effect of digoxin using the H9c2 cell line cultured in high glucose (HG) conditions.
methodsThe effects of digoxin on PPARδ expression, intracellular calcium and TnI phosphorylation were investigated in cultured H9c2 cells, maintained in a HG medium, by using Western blot analysis.
resultsDigoxin increased PPARδ expression in H9c2 cells subjected to HG conditions, and increase the intracellular calcium concentration. This effect of digoxin was blocked by BAPTA-AM at concentrations sufficient to chelate calcium ions. In addition, the calcineurin inhibitor cyclosporine A and KN93, an inhibitor of calcium/calmodulin-dependent protein kinase, inhibited this action. Digoxin also increased TnI phosphorylation and this was inhibited when PPARδ was silenced by the addition of RNAi to the cells. Similar changes were observed on the contraction of H9c2 cells.
conclusionThe results suggest that digoxin appears, through calcium-triggered signals, to reverse the reduced expression of PPARδ in H9c2 cells caused by HG treatment.
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