ArticleThe American journal of pathology1999
Vascular smooth muscle cell proliferation and regrowth after mechanical injury in vitro are Egr-1/NGFI-A-dependent.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Serum-Induced Proliferation of Human Cardiac Stem Cells Is Modulated via TGFβRI/II and SMAD2/3.International journal of molecular sciences · 2024Article
- Flubendazole inhibits PD-1 and suppresses melanoma growth in immunocompetent mice.Journal of translational medicine · 2023Article
- A promising nucleic acid therapy drug: DNAzymes and its delivery system.Frontiers in molecular biosciences · 2023Review
- The extracellular matrix protein mindin attenuates colon cancer progression by blocking angiogenesis via Egr-1-mediated regulation.Oncogene · 2018Article
- Pitavastatin Regulates Ang II Induced Proliferation and Migration via IGFBP-5 in VSMC.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Article
- Crucial role for early growth response-1 in the transcriptional regulation of miR-20b in breast cancer.Oncotarget · 2013Article
- An Egr-1-specific DNAzyme regulates Egr-1 and proliferating cell nuclear antigen expression in rat vascular smooth muscle cells.Experimental and therapeutic medicine · 2013Article
- Egr-1 expression during neointimal development in flow-associated pulmonary hypertension.The American journal of pathology · 2011Article
- Time course analysis of gene expression identifies multiple genes with differential expression in patients with in-stent restenosis.BMC medical genomics · 2011Article
- A key role for early growth response-1 and nuclear factor-kappaB in mediating and maintaining GRO/CXCR2 proliferative signaling in esophageal cancer.Molecular cancer research : MCR · 2009Article
- Transforming growth factor beta1-mediated activation of the smooth muscle alpha-actin gene in human pulmonary myofibroblasts is inhibited by tumor necrosis factor-alpha via mitogen-activated protein kinase kinase 1-dependent induction of the Egr-1 transcriptional repressor.Molecular biology of the cell · 2009Article
- Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells.European journal of pharmacology · 2009Article
- DNAzymes and cardiovascular disease.British journal of pharmacology · 2008Review
- Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury.Current atherosclerosis reports · 2006Review
- Berberine suppresses MEK/ERK-dependent Egr-1 signaling pathway and inhibits vascular smooth muscle cell regrowth after in vitro mechanical injury.Biochemical pharmacology · 2006Article
- Egr-1 is a major vascular pathogenic transcription factor in atherosclerosis and restenosis.Reviews in endocrine & metabolic disorders · 2004Review
- Inhibition of human breast carcinoma proliferation, migration, chemoinvasion and solid tumour growth by DNAzymes targeting the zinc finger transcription factor EGR-1.Nucleic acids research · 2004Article
- Inhibition of Egr-1 expression reverses transformation of prostate cancer cells in vitro and in vivo.Oncogene · 2003Article
- Net-targeted mutant mice develop a vascular phenotype and up-regulate egr-1.The EMBO journal · 2001Article
- Catalytic DNAs as potential therapeutic agents and sequence-specific molecular tools to dissect biological function.The Journal of clinical investigation · 2000Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smooth muscle cell (SMC) proliferation is a key event in renarrowing of blood vessels after balloon angioplasty. Mechanical injury imparted to the arterial wall in experimental models induces the expression of the immediate-early gene, egr-1. Egr-1 binds to and activates expression from the proximal promoters of multiple genes whose products can, in turn, influence the vascular response to injury. Here, we used antisense strategies in vitro to inhibit rat vascular SMC proliferation by directly targeting Egr-1. A series of phosphorothioate antisense oligonucleotides of 15 base length and complementary to various theoretically accessible regions within Egr-1 mRNA were synthesized and assessed for their ability to selectively inhibit SMC proliferation in an Egr-1-dependent manner. Western blot analysis revealed that two oligonucleotides, AS2 and E11, inhibited Egr-1 synthesis in cells exposed to serum without affecting levels of the zinc finger protein Sp1. AS2 and E11 inhibited serum-inducible [(3)H]thymidine incorporation into DNA, as well as serum stimulation of total cell numbers. Size-matched phosphorothioate oligonucleotides with random, scrambled, sense or mismatch sequences failed to inhibit. Antisense Egr-1 inhibition was nontoxic and reversible. These oligonucleotides also inhibited SMC regrowth after mechanical injury in vitro. Egr-1 thus plays a key regulatory role in SMC proliferation and repair following injury.
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