ArticlePloS one2011
Platelet-derived growth factor induces Rad expression through Egr-1 in vascular smooth muscle cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Friend or Foe: Regulation, Downstream Effectors of RRAD in Cancer.Biomolecules · 2023Review
- Ras associated with diabetes may play a role in fracture nonunion development in rats.BMC musculoskeletal disorders · 2019Article
- Elk-3 Contributes to the Progression of Liver Fibrosis by Regulating the Epithelial-Mesenchymal Transition.Gut and liver · 2017Article
- PDGF induces SphK1 expression via Egr-1 to promote pulmonary artery smooth muscle cell proliferation.American journal of physiology. Cell physiology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRas associated with diabetes (Rad) inhibits vascular lesion formation by reducing the attachment and migration of vascular smooth muscle cells (VSMCs). However, the transcriptional regulation of Rad in VSMCs is unclear. METHODOLOGY AND PRINCIPAL
findingsWe found that Platelet-Derived Growth Factor (PDGF)induced Rad expression in a time- and dose-dependent manner in rat aortic smooth muscle cells (RASMCs) using quantitative real-time PCR. By serial deletion analysis of the Rad promoter, we identified that two GC-rich early growth response-1 (Egr-1) binding sites are essential for PDGF-induced Rad promoter activation. Overexpression of Egr-1 in RASMCs strongly stimulated Rad expression while the Egr-1 corepressor, NGFI-A binding protein 2 (NAB2), repressed PDGF-induced Rad up-regulation in a dose-dependent manner. Direct binding of Egr-1 to the Rad promoter region was further confirmed by chromatin immunoprecipitation assays.
conclusionsOur results demonstrate that Rad is regulated by PDGF through the transcriptional factor Egr-1 in RASMCs.
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Registered trials
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