ArticleAmerican journal of respiratory cell and molecular biology2015
Lung-specific loss of α3 laminin worsens bleomycin-induced pulmonary fibrosis.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Molecular plasticity of LAMA3 across the disease spectrum: pathogenic mechanisms and clinical translation.Histochemistry and cell biology · 2026Pooled it
- Proteomic characterization ofVirulence · 2025Article
- Local photocrosslinking of native tissue matrix regulates lung epithelial cell mechanosensing and function.Nature materials · 2025Article
- Basement membranes in lung development, disease, and repair.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- An orally bioavailable BRD4 inhibitor disrupts expansion of a pathogenic epithelial-mesenchymal niche in bleomycin-induced fibrosis.Respiratory research · 2025Article
- Mechanisms on How Matricellular Microenvironments Sustain Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2025Review
- Article
- The correlation between serum levels of laminin, type IV collagen, type III procollagen N-terminal peptide and hyaluronic acid with the progression of post-COVID-19 pulmonary fibrosis.Frontiers in cell and developmental biology · 2024Article
- Crosstalk with lung fibroblasts shapes the growth and therapeutic response of mesothelioma cells.Cell death & disease · 2023Article
- Endothelial-specific loss of IKKβ disrupts pulmonary endothelial angiogenesis and impairs postnatal lung growth.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Correlations between serum laminin level and severity of heart failure in patients with chronic heart failure.Frontiers in cardiovascular medicine · 2023Article
- Serum hyaluronic acid and procollagen III, N-terminal propeptide levels are highly associated with disease severity and predict the progression of COVID-19.Frontiers in cellular and infection microbiology · 2023Article
- Cell-Specific Response of NSIP- and IPF-Derived Fibroblasts to the Modification of the Elasticity, Biological Properties, and 3D Architecture of the Substrate.International journal of molecular sciences · 2022Article
- Laminin N-terminus α31 expression during development is lethal and causes widespread tissue-specific defects in a transgenic mouse model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Genetic determinants of ammonia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Digital Image Analysis of Picrosirius Red Staining: A Robust Method for Multi-Organ Fibrosis Quantification and Characterization.Biomolecules · 2020Article
- Regulation of cellular senescence by extracellular matrix during chronic fibrotic diseases.Clinical science (London, England : 1979) · 2020Review
- Linear ubiquitin assembly complex regulates lung epithelial-driven responses during influenza infection.The Journal of clinical investigation · 2020Article
- Matrisome Properties of Scaffolds Direct Fibroblasts in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2019Article
- Matrix biomechanics and dynamics in pulmonary fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
Abstract
Laminins are heterotrimeric proteins that are secreted by the alveolar epithelium into the basement membrane, and their expression is altered in extracellular matrices from patients with pulmonary fibrosis. In a small number of patients with pulmonary fibrosis, we found that the normal basement membrane distribution of the α3 laminin subunit was lost in fibrotic regions of the lung. To determine if these changes play a causal role in the development of fibrosis, we generated mice lacking the α3 laminin subunit specifically in the lung epithelium by crossing mice expressing Cre recombinase driven by the surfactant protein C promoter (SPC-Cre) with mice expressing floxed alleles encoding the α3 laminin gene (Lama3(fl/fl)). These mice exhibited no developmental abnormalities in the lungs up to 6 months of age, but, compared with control mice, had worsened mortality, increased inflammation, and increased fibrosis after the intratracheal administration of bleomycin. Similarly, the severity of fibrosis induced by an adenovirus encoding an active form of transforming growth factor-β was worse in mice deficient in α3 laminin in the lung. Taken together, our results suggest that the loss of α3 laminin in the lung epithelium does not affect lung development, but plays a causal role in the development of fibrosis in response to bleomycin or adenovirally delivered transforming growth factor-β. Thus, we speculate that the loss of the normal basement membrane organization of α3 laminin that we observe in fibrotic regions from the lungs of patients with pulmonary fibrosis contributes to their disease progression.
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