ArticleAnnals of the rheumatic diseases2005
Inhibition of collagen gene expression in systemic sclerosis dermal fibroblasts by mithramycin.
Article in Annals of the rheumatic diseases, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 1 citations in OpenAlex.
- Identification of Potential ceRNA Network and Patterns of Immune Cell Infiltration in Systemic Sclerosis-Associated Interstitial Lung Disease.Frontiers in cell and developmental biology · 2021Article
- Egr-1 mediates low-dose arecoline induced human oral mucosa fibroblast proliferation via transactivation of Wnt5a expression.BMC molecular and cell biology · 2020Article
- Article
- Matrix remodeling in systemic sclerosis.Seminars in immunopathology · 2015Review
- Sp1king out cancer (....and fibrosis?).Journal of cell communication and signaling · 2012Article
- Mithramycin reduces expression of fibro-proliferative mRNAs in human gingival fibroblasts.Cell proliferation · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe anti-tumour antibiotic mithramycin is also a potent inhibitor of fibrosis after glaucoma surgery. This drug displays high affinity binding to GC-rich sequences in DNA, including those present in the promoter of the gene encoding the alpha1 chain of type I collagen (COL1A1).
objectiveTo evaluate the effects of mithramycin on COL1A1 expression in systemic sclerosis fibroblasts.
methodsConfluent cultures of dermal fibroblasts from patients with recent onset diffuse systemic sclerosis were treated with mithramycin in vitro. Cell viability and protein expression were examined by fluorescence and confocal imaging. Type I collagen production was analysed by confocal imaging and metabolic labelling. COL1A1 messenger RNA levels and stability were assessed by northern hybridisation, and COL1A1 transcription was examined by transient transfections.
resultsTreatment of systemic sclerosis fibroblasts with mithramycin (10-100 nmol/l) did not cause significant cytotoxicity. Type I collagen biosynthesis decreased by 33-40% and 50-70% in cells cultured with mithramycin at 10 nmol/l and 100 nmol/l, respectively. Mithramycin at 50 nmol/l decreased COL1A1 mRNA levels by 40-60%. The effects of mithramycin on collagen gene expression were mediated by transcriptional and post-transcriptional mechanisms as shown by the reduction of COL1A1 promoter activity and by a decrease in the stability of these transcripts, respectively.
conclusionsMithramycin causes potent inhibition of collagen production and gene expression in systemic sclerosis dermal fibroblasts in vitro in the absence of cytotoxic effects. These results suggest that this drug may be an effective treatment for the fibrotic process which is the hallmark of systemic sclerosis.
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