ArticleThe American journal of pathology1999
Early growth response factor-1 induction by injury is triggered by release and paracrine activation by fibroblast growth factor-2.
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 30 papers.
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Who cites it
30 citing papers in PubMed, 114 citations in OpenAlex.
- Preemptive cardioprotection with a small molecule in rodents that suppresses genes predictive of heart failure.Science advances · 2026Article
- A Comprehensive Bibliometric and Visual Analysis of EGR1 in Cardiovascular Disease.Molecular biotechnology · 2026Review
- Effects of Late-Passage Small Umbilical Cord-Derived Fast Proliferating Cells on Tenocytes from Degenerative Rotator Cuff Tears under an Interleukin 1β-Induced Tendinopathic Environment.Tissue engineering and regenerative medicine · 2024Article
- Angiogenic gene networks are dysregulated in opioid use disorder: evidence from multi-omics and imaging of postmortem human brain.Molecular psychiatry · 2021Article
- Early Growth Response-1, an Integrative Sensor in Cardiovascular and Inflammatory Disease.Journal of the American Heart Association · 2021Review
- Serine 26 in Early Growth Response-1 Is Critical for Endothelial Proliferation, Migration, and Network Formation.Journal of the American Heart Association · 2021Article
- Egr-1 regulates irradiation-induced autophagy through Atg4B to promote radioresistance in hepatocellular carcinoma cells.Oncogenesis · 2017Article
- Transcriptional regulation of tumour necrosis factor-related apoptosis-inducing ligand.Cellular and molecular life sciences : CMLS · 2013Review
- Crucial role for early growth response-1 in the transcriptional regulation of miR-20b in breast cancer.Oncotarget · 2013Article
- Marine algal carotenoids inhibit angiogenesis by down-regulating FGF-2-mediated intracellular signals in vascular endothelial cells.Molecular and cellular biochemistry · 2013Article
- Suppression of transcription factor early growth response 1 reduces herpes simplex virus 1-induced corneal disease in mice.Journal of virology · 2012Article
- Hypochlorite-modified high-density lipoprotein promotes induction of HO-1 in endothelial cells via activation of p42/44 MAPK and zinc finger transcription factor Egr-1.Archives of biochemistry and biophysics · 2011Article
- The role of FGF-2 and BMP-2 in regulation of gene induction, cell proliferation and mineralization.Journal of orthopaedic surgery and research · 2011Article
- Article
- Egr-1 is necessary for fibroblast growth factor-2-induced transcriptional activation of the glial cell line-derived neurotrophic factor in murine astrocytes.The Journal of biological chemistry · 2009Article
- The fibrotic phenotype induced by IGFBP-5 is regulated by MAPK activation and egr-1-dependent and -independent mechanisms.The American journal of pathology · 2009Article
- DNAzymes and cardiovascular disease.British journal of pharmacology · 2008Review
- Involvement of MAPK/ERK kinase-ERK pathway in exogenous bFGF-induced Egr-1 binding activity enhancement in anoxia-reoxygenation injured astrocytes.Neuroscience bulletin · 2007Article
- Induction of transcription factor Egr-1 gene expression in astrocytoma cells by Murine coronavirus infection.Virology · 2006Article
- Induction of the early growth response 1 gene by Epstein-Barr virus lytic transactivator Zta.Journal of virology · 2006Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell migration and proliferation that follows injury to the artery wall is preceded by signaling and transcriptional events that converge at the promoters of multiple genes whose products can influence formation of the neointima. Transcription factors, such as early growth response factor-1 (Egr-1), with nucleotide recognition elements in the promoters of many pathophysiologically relevant genes, are expressed at the endothelial wound edge within minutes of injury. The mechanisms underlying the inducible expression of Egr-1 in this setting are not clear. Understanding this process would provide important mechanistic insights into the earliest events in the response to injury. In this report, we demonstrate that fibroblast growth factor-2 (FGF-2) is released by injury and that antibodies to FGF-2 almost completely abrogate the activation and nuclear accumulation of Egr-1. FGF-2-inducible egr-1-promoter-dependent expression is blocked by PD98059, a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK)-1/2 (MEK-1/2), as well as by dominant negative mutants of ERK-1/2. Inducible ERK phosphorylation after injury is dependent on release and stimulation by endogenous FGF-2. Antisense oligonucleotides directed at egr-1 mRNA suggest that Egr-1 plays a necessary role in endothelial repair after denudation of the monolayer. These findings demonstrate that inducible Egr-1 expression after injury is contingent on the release and paracrine action of FGF-2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.