ArticleThe Journal of clinical investigation2000
Suppressed smooth muscle proliferation and inflammatory cell invasion after arterial injury in elafin-overexpressing mice.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 51 citations in OpenAlex.
- Perioperative elafin for ischaemia-reperfusion injury during coronary artery bypass graft surgery: a randomised-controlled trial.Heart (British Cardiac Society) · 2015Trial
- Serum elafin levels in patients with IgA vasculitis: a prospective case-control study.Pediatric rheumatology online journal · 2025Article
- New and Emerging Therapies for Pulmonary Arterial Hypertension.Annual review of medicine · 2019Review
- BMP type II receptor as a therapeutic target in pulmonary arterial hypertension.Cellular and molecular life sciences : CMLS · 2017Review
- WFDC1 is a key modulator of inflammatory and wound repair responses.The American journal of pathology · 2014Article
- Gene expression profiling on the molecular action of danshen-gegen formula in a randomized placebo-controlled trial of postmenopausal women with hypercholesterolemia.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Neonatal mice genetically modified to express the elastase inhibitor elafin are protected against the adverse effects of mechanical ventilation on lung growth.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- AMPKα2 deletion exacerbates neointima formation by upregulating Skp2 in vascular smooth muscle cells.Circulation research · 2011Article
- Neutrophil elastase is produced by pulmonary artery smooth muscle cells and is linked to neointimal lesions.The American journal of pathology · 2011Article
- Inhibiting lung elastase activity enables lung growth in mechanically ventilated newborn mice.American journal of respiratory and critical care medicine · 2011Article
- Extracellular matrix degradation products and low-oxygen conditions enhance the regenerative potential of perivascular stem cells.Tissue engineering. Part A · 2011Article
- Evolution of trappin genes in mammals.BMC evolutionary biology · 2010Article
- Expression profiles of elastase1 (NvElastaseI) and secretory leukocyte protease inhibitor (NvSLPI) during forelimb regeneration in adult Notophthalmus viridescens suggest a role in epithelial remodeling and delamination.Development genes and evolution · 2006Article
- Integration of flow-dependent endothelial phenotypes by Kruppel-like factor 2.The Journal of clinical investigation · 2006Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elastases degrade the extracellular matrix, releasing growth factors and chemotactic peptides, inducing glycoproteins such as tenascin, and thereby promoting vascular cell proliferation and migration. Administration of serine elastase inhibitors reduces experimentally induced vascular disease. The ability to mount an intrinsic anti-elastase response may, therefore, protect against intimal/medial thickening after vascular injury. To investigate this, we showed that wire-induced endothelial denudation of the carotid artery is associated with transient elevation in elastase activity and confirmed that this is abolished in transgenic mice overexpressing the serine elastase inhibitor, elafin, targeted to the cardiovascular system. Ten days after injury, nontransgenic littermates show vessel enlargement, intimal thickening, increased medial area and cellularity, and 2-fold increase in tenascin. Injured vessels in transgenic mice become enlarged but are otherwise similar to sham-operated controls. Injury-induced vessel wall thickening, which is observed only in nontransgenic mice, is related to foci of neutrophils and macrophages, in addition to smooth muscle cells that fail to stain for alpha-actin and are likely dedifferentiated. Our study therefore suggests that a major determinant of the vascular response to injury is the early transient induction of serine elastase activity, which leads to cellular proliferation and inflammatory cell migration.
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Registered trials
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.