ArticleThe American journal of pathology1998
Gelatinases A and B are up-regulated in rat lungs by subacute hyperoxia: pathogenetic implications.
Article in The American journal of pathology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 103 citations in OpenAlex.
- Tissue Inhibitor of Matrix Metalloproteinases-1 (TIMP-1) and Pulmonary Involvement in COVID-19 Pneumonia.Biomolecules · 2023Article
- An aberrant STAT pathway is central to COVID-19.Cell death and differentiation · 2020Review
- Role of Nrf2 in inflammatory response in lung of mice exposed to zinc oxide nanoparticles.Particle and fibre toxicology · 2019Article
- The Versatile Role of Matrix Metalloproteinase for the Diverse Results of Fibrosis Treatment.Molecules (Basel, Switzerland) · 2019Review
- Reactive Oxygen Species, Biomarkers of Microvascular Maturation and Alveolarization, and Antioxidants in Oxidative Lung Injury.Reactive oxygen species (Apex, N.C.) · 2018Article
- IL-33 Can Promote the Process of Pulmonary Fibrosis by Inducing the Imbalance Between MMP-9 and TIMP-1.Inflammation · 2018Article
- The Extracellular Matrix in Bronchopulmonary Dysplasia: Target and Source.Frontiers in medicine · 2015Review
- The role of intrinsic pathway in apoptosis activation and progression in Peyronie's disease.BioMed research international · 2014Article
- Article
- Cyclic stretch-induced oxidative stress increases pulmonary alveolar epithelial permeability.American journal of respiratory cell and molecular biology · 2013Article
- Effects of a superoxide dismutase mimetic on biomarkers of lung angiogenesis and alveolarization during hyperoxia with intermittent hypoxia.American journal of translational research · 2013Article
- Diospyros blancoi attenuates asthmatic effects in a mouse model of airway inflammation.Inflammation · 2012Article
- Article
- A role for matrix metalloproteinase 9 in IFNγ-mediated injury in developing lungs: relevance to bronchopulmonary dysplasia.American journal of respiratory cell and molecular biology · 2011Article
- Retinoic acid diminished the expression of MMP-2 in hyperoxia-exposed premature rat lung fibroblasts through regulating mitogen-activated protein kinases.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2011Article
- Long-term alcohol consumption increases pro-matrix metalloproteinase-9 levels via oxidative stress.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2010Article
- MICA polymorphisms and decreased expression of the MICA receptor NKG2D contribute to idiopathic pulmonary fibrosis susceptibility.Human genetics · 2009Article
- Early and late changes of MMP-2 and MMP-9 in bleomycin-induced pulmonary fibrosis.Yonsei medical journal · 2009Article
- Role of matrix metalloprotease-9 in hyperoxic injury in developing lung.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- The role of proteoglycans in pulmonary edema development.Intensive care medicine · 2008Review
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Subacute hyperoxia may cause basement membrane disruption and subsequent fibrosis. To test the role of extracellular matrix degradation in hyperoxic damage, we analyzed the expression of gelatinases A and B and tissue inhibitors of metalloproteinases (TIMP)-1 and TIMP-2 in rats exposed to 85% O2. Oxygen-exposed rats were studied at 1, 3, 5, and 7 days, and compared with air-breathing rats. Lung mRNAs assayed by Northern and in situ hybridization showed an up-regulation of lung gelatinases A and B from the 3rd day on. Gelatinase A was localized in alveolar macrophages and in interstitial and alveolar epithelial cells. Gelatinase B mRNA and protein were localized in macrophages and bronchiolar and alveolar epithelial cells. Increased gelatinase A and B activities were demonstrated in bronchoalveolar lavage. TIMP-1 and TIMP-2 were constitutively expressed, and only TIMP-1 displayed a moderate increase with hyperoxia. To elucidate transcriptional mechanisms for increased gelatinase B expression after hyperoxia, nuclear transcription factor-kappabeta activation was explored. Oxidative stress significantly increased the lung expression of nuclear transcription factor-kappabeta (p65) protein, and nuclear transcription factor-kappabeta activation and increased levels of gelatinases A and B were found in isolated type II alveolar cells obtained from hyperoxic rats. Conceivably, subacute hyperoxia induces excessive gelatinase activity, which may contribute to lung damage.
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