ArticleThe American journal of pathology2011
Egr-1 expression during neointimal development in flow-associated pulmonary hypertension.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Pulmonary Vascular Signaling in Pulmonary Hypertension: Potential Role of Endothelial CaArteriosclerosis, thrombosis, and vascular biology · 2026Review
- Transgelin exacerbates pulmonary artery smooth muscle cell dysfunction in shunt-related pulmonary arterial hypertension.ESC heart failure · 2022Article
- Computational simulation-derived hemodynamic and biomechanical properties of the pulmonary arterial tree early in the course of ventricular septal defects.Biomechanics and modeling in mechanobiology · 2021Article
- Animal models of right heart failure.Cardiovascular diagnosis and therapy · 2020Review
- Hyperglycaemia cause vascular inflammation through advanced glycation end products/early growth response-1 axis in gestational diabetes mellitus.Molecular and cellular biochemistry · 2019Article
- Characteristics of Pulmonary Vascular Remodeling in a Novel Model of Shunt-Associated Pulmonary Arterial Hypertension.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Egr-1 mediates leptin-induced PPARγ reduction and proliferation of pulmonary artery smooth muscle cells.Molecular biology of the cell · 2018Article
- Shunt Surgery, Right Heart Catheterization, and Vascular Morphometry in a Rat Model for Flow-induced Pulmonary Arterial Hypertension.Journal of visualized experiments : JoVE · 2017Article
- Aberrant gene expression of heparanase in ventricular hypertrophy induced by monocrotaline in rats.The Journal of veterinary medical science · 2016Article
- Endothelial Plasticity: Shifting Phenotypes through Force Feedback.Stem cells international · 2016Review
- Erythropoietin Attenuates Pulmonary Vascular Remodeling in Experimental Pulmonary Arterial Hypertension through Interplay between Endothelial Progenitor Cells and Heme Oxygenase.Frontiers in pediatrics · 2015Article
- Pulmonary hypertension caused by pulmonary venous hypertension.Pulmonary circulation · 2014Review
- Egr-1: new conductor for the tissue repair orchestra directs harmony (regeneration) or cacophony (fibrosis).The Journal of pathology · 2013Review
- Transfected early growth response gene-1 DNA enzyme prevents stenosis and occlusion of autogenous vein graft in vivo.BioMed research international · 2013Article
- Inhibition of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) reverses experimental pulmonary hypertension.The Journal of experimental medicine · 2012Article
- Pulmonary blood flow and pulmonary hypertension: Is the pulmonary circulation flowophobic or flowophilic?Pulmonary circulation · 2012Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In flow-associated pulmonary arterial hypertension (PAH), increased pulmonary blood flow is an essential trigger for neointimal formation. Using microarray analysis, we recently found that the early growth response protein 1 (Egr-1) transcription factor is increased in experimental flow-associated end-stage PAH. Its role in PAH development is unknown. Here, we assessed the spatiotemporal expression of Egr-1 during neointimal development in flow-associated PAH. Flow-associated PAH was produced in rats by combining monocrotaline administration with an aortocaval shunt. Animals were sacrificed 1 day before or 1 day, 1 week, or 4 to 5 weeks after flow addition. Egr-1 expression was spatiotemporally assessed using laser microdissection, quantitative real-time PCR and immunohistochemistry. In addition, Egr-1 expression was assessed in a non-neointimal pulmonary hypertension model and in human PAH associated with congenital shunt. In 4 to 5 weeks, rats subjected to increased flow developed PAH with neointimal lesions. Egr-1 mRNA was increased 1 day after flow addition and in end-stage PAH, whereas monocrotaline only did not result in increased Egr-1 mRNA. Directly after flow addition, Egr-1 was expressed in endothelial cells. During disease development, Egr-1 protein expression increased and migrated throughout the vessel wall. In PAH patients, Egr-1 was expressed in vessels with media hypertrophy and neointimal lesions, including plexiform lesions. Thus, Egr-1 may be an important regulator in the development of pulmonary neointimal lesions induced by increased pulmonary blood flow.
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