ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
Role of matrix metalloprotease-9 in hyperoxic injury in developing lung.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. 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, 66 citations in OpenAlex.
- Defining endotypes of bronchopulmonary dysplasia in preterm infants to improve precision-based therapies.JCI insight · 2025Review
- Anti-CELA1 antibody KF4 prevents emphysema by inhibiting stretch-mediated remodeling.JCI insight · 2024Article
- CXCL10 deficiency limits macrophage infiltration, preserves lung matrix, and enables lung growth in bronchopulmonary dysplasia.Inflammation and regeneration · 2023Article
- Hyperoxia-induced bronchopulmonary dysplasia: better models for better therapies.Disease models & mechanisms · 2021Review
- Early Plasma Matrix Metalloproteinase Profiles. A Novel Pathway in Pediatric Acute Respiratory Distress Syndrome.American journal of respiratory and critical care medicine · 2019Article
- A Pathogenic Relationship of Bronchopulmonary Dysplasia and Retinopathy of Prematurity? A Review of Angiogenic Mediators in Both Diseases.Frontiers in pediatrics · 2018Review
- A purinergic P2Y6 receptor agonist prodrug modulates airway inflammation, remodeling, and hyperreactivity in a mouse model of asthma.Journal of asthma and allergy · 2018Article
- Ureaplasma isolates stimulate pro-inflammatory CC chemokines and matrix metalloproteinase-9 in neonatal and adult monocytes.PloS one · 2018Article
- Moderate hyperoxia induces extracellular matrix remodeling by human fetal airway smooth muscle cells.Pediatric research · 2017Article
- Correlation of matrix metalloproteinase-2 and -9 expression with recurrences in primary spontaneous pneumothorax patients.Journal of thoracic disease · 2016Article
- Gene expression profile in newborn rat lungs after two days of recovery of mechanical ventilation.Pediatric research · 2015Article
- Pigment epithelium-derived factor mediates impaired lung vascular development in neonatal hyperoxia.American journal of respiratory cell and molecular biology · 2015Article
- The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source.Frontiers in medicine · 2015Review
- Superoxide dismutase 3 dysregulation in a murine model of neonatal lung injury.American journal of respiratory cell and molecular biology · 2014Article
- Indacaterol inhibits tumor cell invasiveness and MMP-9 expression by suppressing IKK/NF-κB activation.Molecules and cells · 2014Article
- Transient vascular and long-term alveolar deficits following a hyperoxic injury to neonatal mouse lung.BMC pulmonary medicine · 2014Article
- Lung development alterations in newborn mice after recovery from exposure to sublethal hyperoxia.The American journal of pathology · 2014Article
- Postnatal inflammation in the pathogenesis of bronchopulmonary dysplasia.Birth defects research. Part A, Clinical and molecular teratology · 2014Review
- Chronic lung disease in the preterm infant. Lessons learned from animal models.American journal of respiratory cell and molecular biology · 2014Review
- VARA attenuates hyperoxia-induced impaired alveolar development and lung function in newborn mice.American journal of physiology. Lung cellular and molecular physiology · 2013Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Matrix metalloprotease-9 (MMP-9) is increased in lung injury following hyperoxia exposure in neonatal mice, in association with impaired alveolar development. We studied the role of MMP-9 in the mechanism of hyperoxia-induced functional and histological changes in neonatal mouse lung. Reduced alveolarization with remodeling of ECM is a major morbidity component of oxidant injury in developing lung. MMP-9 mediates oxidant injury in developing lung causing altered lung remodeling. Five-day-old neonatal wild-type (WT) and MMP-9 (-/-) mice were exposed to hyperoxia for 8 days. The lungs were inflation fixed, and sections were examined for morphometry. The mean linear intercept and alveolar counts were evaluated. Immunohistochemistry for MMP-9 and elastin was performed. MMP-2, MMP-9, type I collagen, and tropoelastin were measured by Western blot analysis. Lung quasistatic compliance was studied in anaesthetized mice. MMP-2 and MMP-9 were significantly increased in lungs of WT mice exposed to hyperoxia compared with controls. Immunohistochemistry showed an increase in MMP-9 in mesenchyme and alveolar epithelium of hyperoxic lungs. The lungs of hyperoxia-exposed WT mice had less gas exchange surface area and were less compliant compared with room air-exposed WT and hyperoxia-exposed MMP-9 (-/-) mice. Type I collagen and tropoelastin were increased in hyperoxia-exposed WT with aberrant elastin staining. These changes were ameliorated in hyperoxia-exposed MMP-9 (-/-) mice. MMP-9 plays an important role in the structural changes consequent to oxygen-induced lung injury. Blocking MMP-9 activity may lead to novel therapeutic approaches in preventing bronchopulmonary dysplasia.
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