ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Deregulation of the lysyl hydroxylase matrix cross-linking system in experimental and clinical bronchopulmonary dysplasia.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Impaired myofibroblast proliferation is a central feature of pathologic post-natal alveolar simplification.eLife · 2024Article
- Impaired Myofibroblast Proliferation is a Central Feature of Pathologic Post-Natal Alveolar Simplification.bioRxiv : the preprint server for biology · 2024Article
- Nitric oxide regulation of fetal and newborn lung development and function.Nitric oxide : biology and chemistry · 2024Review
- CXCL10 deficiency limits macrophage infiltration, preserves lung matrix, and enables lung growth in bronchopulmonary dysplasia.Inflammation and regeneration · 2023Article
- Development of a blood proteins-based model for bronchopulmonary dysplasia prediction in premature infants.BMC pediatrics · 2023Article
- Lysyl oxidase regulation and protein aldehydes in the injured newborn lung.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Sphingosine kinase 1 regulates lysyl oxidase through STAT3 in hyperoxia-mediated neonatal lung injury.Thorax · 2022Article
- Established severe BPD: is there a way out? Change of ventilatory paradigms.Pediatric research · 2021Review
- The critical role of collagen VI in lung development and chronic lung disease.Matrix biology plus · 2021Review
- Hyperoxia and Lungs: What We Have Learned From Animal Models.Frontiers in medicine · 2021Review
- Signaling Pathways Involved in the Development of Bronchopulmonary Dysplasia and Pulmonary Hypertension.Children (Basel, Switzerland) · 2020Review
- Extracellular matrix in lung development, homeostasis and disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Article
- The Potentials and Caveats of Mesenchymal Stromal Cell-Based Therapies in the Preterm Infant.Stem cells international · 2018Review
- LungMAP: The Molecular Atlas of Lung Development Program.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- Looking ahead: where to next for animal models of bronchopulmonary dysplasia?Cell and tissue research · 2017Review
- Pathogenesis of bronchopulmonary dysplasia: when inflammation meets organ development.Molecular and cellular pediatrics · 2016Review
- Searching for better animal models of BPD: a perspective.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- The roles of Tenascin C and Fibronectin 1 in adhesive capsulitis: a pilot gene expression study.Clinics (Sao Paulo, Brazil) · 2016Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Bronchopulmonary dysplasia (BPD) is a common and serious complication of premature birth, characterized by a pronounced arrest of alveolar development. The underlying pathophysiological mechanisms are poorly understood although perturbations to the maturation and remodeling of the extracellular matrix (ECM) are emerging as candidate disease pathomechanisms. In this study, the expression and regulation of three members of the lysyl hydroxylase family of ECM remodeling enzymes (Plod1, Plod2, and Plod3) in clinical BPD, as well as in an experimental animal model of BPD, were addressed. All three enzymes were localized to the septal walls in developing mouse lungs, with Plod1 also expressed in the vessel walls of the developing lung and Plod3 expressed uniquely at the base of developing septa. The expression of plod1, plod2, and plod3 was upregulated in the lungs of mouse pups exposed to 85% O2, an experimental animal model of BPD. Transforming growth factor (TGF)-β increased plod2 mRNA levels and activated the plod2 promoter in vitro in lung epithelial cells and in lung fibroblasts. Using in vivo neutralization of TGF-β signaling in the experimental animal model of BPD, TGF-β was identified as the regulator of aberrant plod2 expression. PLOD2 mRNA expression was also elevated in human neonates who died with BPD or at risk for BPD, compared with neonates matched for gestational age at birth or chronological age at death. These data point to potential roles for lysyl hydroxylases in normal lung development, as well as in perturbed late lung development associated with BPD.
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Registered trials
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