ArticleAmerican journal of physiology. Lung cellular and molecular physiology2007
Mechanisms of induction of airway smooth muscle hyperplasia by transforming growth factor-beta.
Article in American journal of physiology. Lung cellular and molecular physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 112 citations in OpenAlex.
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- Selective HDAC8 inhibition by PCI-34051 attenuates inflammation and airway remodeling in asthmaJournal of translational internal medicine · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Elevated Proportions of Circulating CXCR5Journal of immunology research · 2024Article
- Review
- Bronchial smooth muscle cell in asthma: where does it fit?BMJ open respiratory research · 2022Review
- MicroRNA-21 inhibition attenuates airway inflammation and remodelling by modulating the transforming growth factor β-Smad7 pathway.The Korean journal of internal medicine · 2021Article
- TGF-β: The missing link in obesity-associated airway diseases?Current research in pharmacology and drug discovery · 2021Review
- HMGB1 amplifies ILC2-induced type-2 inflammation and airway smooth muscle remodelling.PLoS pathogens · 2020Article
- Action of 1,25(OH)Journal of asthma and allergy · 2020Article
- Navigating the disease landscape: knowledge representations for contextualizing molecular signatures.Briefings in bioinformatics · 2019Review
- High mobility group protein B1 (HMGB1) interacts with receptor for advanced glycation end products (RAGE) to promote airway smooth muscle cell proliferation through ERK and NF-International journal of clinical and experimental pathology · 2019Article
- Fibroblast-to-myofibroblast transition in bronchial asthma.Cellular and molecular life sciences : CMLS · 2018Review
- Roles of airway smooth muscle dysfunction in chronic obstructive pulmonary disease.Journal of translational medicine · 2018Review
- New targets for resolution of airway remodeling in obstructive lung diseases.F1000Research · 2018Review
- Therapeutic Effects of Kangzhi Syrup in a Guinea Pig Model of Ovalbumin-Induced Cough Variant Asthma.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- Airway remodeling in asthma: what really matters.Cell and tissue research · 2017Review
- Airway Remodeling in Chronic Obstructive Pulmonary Disease and Asthma: the Role of Matrix Metalloproteinase-9.Archivum immunologiae et therapiae experimentalis · 2016Review
- Association of transforming growth factor-Beta 1 promoter variant -509 c/t with bronchial asthma in South Indian population.Inflammation · 2015Article
- Roxithromycin treatment inhibits TGF-β1-induced activation of ERK and AKT and down-regulation of caveolin-1 in rat airway smooth muscle cells.Respiratory research · 2014Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Airway smooth muscle (ASM) hyperplasia is a characteristic feature of the asthmatic airway, but the underlying mechanisms that induce ASM hyperplasia remain unknown. Because transforming growth factor (TGF)-beta is a potent regulator of ASM cell proliferation, we determined its expression and mitogenic signaling pathways in ASM cells. We obtained ASM cells by laser capture microdissection of bronchial biopsies and found that ASM cells from asthmatic patients expressed TGF-beta1 mRNA and protein to a greater extent than nonasthmatic individuals using real-time RT-PCR and immunohistochemistry, respectively. TGF-beta1 stimulated the growth of nonconfluent and confluent ASM cells either in the presence or absence of serum in a time- and concentration-dependent manner. The mitogenic activity of TGF-beta1 on ASM cells was inhibited by selective inhibitors of TGF-beta receptor I kinase (SD-208), phosphatidylinositol 3-kinase (PI3K, LY-294002), ERK (PD-98059), JNK (SP-600125), and NF-kappaB (AS-602868). On the other hand, p38 MAPK inhibitor (SB-203580) augmented TGF-beta1-induced proliferation. To study role of the Smads, we transduced ASM cells with an adenovirus vector-expressing Smad4, Smad7, or dominant-negative Smad3 and found no involvement of these Smads in TGF-beta1-induced proliferation. Dexamethasone caused a dose-dependent inhibition in TGF-beta1-induced proliferation. Our findings suggest that TGF-beta1 may act in an autocrine fashion to induce ASM hyperplasia, mediated by its receptor and several kinases including PI3K, ERK, and JNK, whereas p38 MAPK is a negative regulator. NF-kappaB is also involved in the TGF-beta1 mitogenic signaling, but Smad pathway does not appear important.
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