ArticleAmerican journal of respiratory cell and molecular biology2011
Genomic differences distinguish the myofibroblast phenotype of distal lung fibroblasts from airway fibroblasts.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- A2BAR Antagonism Mitigates Pulmonary Inflammation and Fibrosis and Restores Macrophage M1/M2 Balance in Diabetic Rats.International journal of molecular sciences · 2026Article
- Ablation of lysophosphatidic acid receptor 1 attenuates hypertrophic cardiomyopathy in a mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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- TWIST1 DNA methylation is a cell marker of airway and parenchymal lung fibroblasts that are differentially methylated in asthma.Clinical epigenetics · 2020Article
- Alveolar wars: The rise of in vitro models to understand human lung alveolar maintenance, regeneration, and disease.Stem cells translational medicine · 2020Review
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- Nascent Lung Organoids Reveal Epithelium- and Bone Morphogenetic Protein-mediated Suppression of Fibroblast Activation.American journal of respiratory cell and molecular biology · 2019Article
- Cultured Human Adipose Tissue Pericytes and Mesenchymal Stromal Cells Display a Very Similar Gene Expression Profile.Stem cells and development · 2015Article
- Lipoxin A4 Attenuates Constitutive and TGF-β1-Dependent Profibrotic Activity in Human Lung Myofibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Matrix, mesenchyme, and mechanotransduction.Annals of the American Thoracic Society · 2015Review
- Human lung myofibroblast TGFβ1-dependent Smad2/3 signalling is Ca(2+)-dependent and regulated by KCa3.1 K(+) channels.Fibrogenesis & tissue repair · 2015Article
- Increased constitutive αSMA and Smad2/3 expression in idiopathic pulmonary fibrosis myofibroblasts is KCa3.1-dependent.Respiratory research · 2014Article
- Network analysis of breast cancer progression and reversal using a tree-evolving network algorithm.PLoS computational biology · 2014Article
- Integrated genomic and prospective clinical studies show the importance of modular pleiotropy for disease susceptibility, diagnosis and treatment.Genome medicine · 2014Article
- Glycogen synthase kinase-3 (GSK-3) regulates TGF-β₁-induced differentiation of pulmonary fibroblasts.British journal of pharmacology · 2013Article
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- Severe asthma: lessons learned from the National Heart, Lung, and Blood Institute Severe Asthma Research Program.American journal of respiratory and critical care medicine · 2012Article
- Redirecting valvular myofibroblasts into dormant fibroblasts through light-mediated reduction in substrate modulus.PloS one · 2012Article
- Regional heterogeneity in murine lung fibroblasts from normal mice or mice exposed once to cigarette smoke.PloS one · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Primary human distal lung/parenchymal fibroblasts (DLFs) exhibit a different phenotype from airway fibroblasts (AFs), including the expression of high levels of α-smooth muscle actin (α-SMA). The scope of the differences between these anatomically differentiated fibroblasts, or the mechanisms driving them, has remained unknown. To determine whether the different characteristics of regional fibroblasts are predicted by distinct genomic differences in AFs versus DLFs, matched human fibroblast pairs were isolated from proximal and distal lung tissue and evaluated. Microarray analysis was performed on 12 matched fibroblast pairs (four normal and eight asthmatic samples) and validated by quantitative real-time PCR. The potential functional implications of these differences were analyzed using computational approaches. Four hundred seventy-four transcripts were up-regulated in AFs, and 611 were up-regulated in DLFs via microarray analysis. No differences in normal and asthmatic fibroblasts were evident, and the data were combined for subsequent analyses. Gene ontology and network analyses suggested distinct patterns of pathway activation between AFs and DLFs. The up-regulation of extracellular matrix-associated molecules in AFs was observed, whereas genes associated with actin binding and cytoskeletal organization were up-regulated in DLFs. The up-regulation of activated/total SMAD3 and c-Jun N-terminal kinase in DLFs may partly explain these myofibroblast-like characteristics in DLFs. Thus, marked genomic differences exist between these two populations of regional lung fibroblasts. These striking differences may help identify potential mechanisms by which AFs and DLFs differ in their responses to injury, regeneration, and remodeling in the lung.
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