Amphotericin B-copper (II) complex alters transcriptional activity of genes encoding transforming growth factor-beta family members and related proteins in renal cells.
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Background Several chemical modifications have been developed to overcome the toxicity of amphotericin B (AmB). Oxidized forms of AmB (AmB-ox), which may occur in patient’s circulation during therapy, are as toxic as AmB. Complexes with copper (II) ions (AmB–Cu2+) have been reported to be less toxic to human cells. Previous studies showed that AmB changed the expression of transforming growth factor-beta (TGF-β). Therefore, the objective of this study was to investigate the influence of AmB and its modified forms on the expression of genes encoding for TGF-β family members and related proteins in renal cells. Methods Human renal proximal tubule cells (RPTEC) were treated with AmB–Cu2+, AmB, or the oxidized form AmB–ox. The expression of TGF-β family members and related genes was determined using oligonucleotide microarrays. TGF-β1 protein level was determined using ELISA method. The mRNA level of TGF-β isoforms, TGF-β receptors and differentiating genes was evaluated by real-time RT-qPCR. Results AmB–Cu2+ increased the mRNA levels of TGF-β1 and TGF-β2 isoforms and two genes encoding receptors: TGFBR1 and TGFBR2. TGF-β1 protein level in culture medium was not increased after stimulation with AmB–Cu2+. Microarray analysis revealed changes in both pro-fibrotic and anti-fibrotic genes. Conclusions These results suggest that AmB–Cu2+ may induce repair mechanisms in renal proximal tubule cells via changes in the expression of genes involved in intracellular signaling.
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Rekord utworzony: | 17 listopada 2017 08:49 |
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Ostatnia aktualizacja: | 28 kwietnia 2021 08:22 |