ArticleRespiratory research2006
TGF-beta1 increases proliferation of airway smooth muscle cells by phosphorylation of map kinases.
Article in Respiratory research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- A molecular systems architecture of asthma.Frontiers in immunology · 2026Pooled it
- Genetic background influences developmental airway smooth muscle program and susceptibility to airway hyperresponsiveness in mice.JCI insight · 2026Article
- E3 ligase RNF145 regulates airway smooth muscle cell proliferation via the PP2A-p70S6K signaling axis.The Journal of biological chemistry · 2026Article
- Computational Investigation of Smooth Muscle Cell Plasticity in Atherosclerosis and Vascular Calcification: Insights from Differential Gene Expression Analysis of Microarray Data.Bioengineering (Basel, Switzerland) · 2025Article
- Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice.bioRxiv : the preprint server for biology · 2025Article
- Syndecan-4 promotes gastric cancer progression through activating TGF-β1 induced lipid reprogramming and contributes positive loop circuits.Discover oncology · 2025Article
- Increased Serum EphA2 is Associated with Disease Severity in Pediatric Patients with Asthma.Journal of asthma and allergy · 2025Article
- Nasal allergen and methacholine provocation tests influence co‑expression patterns of TGF‑β/SMAD and MAPK signaling pathway genes in patients with asthma.Experimental and therapeutic medicine · 2024Article
- Selective HDAC8 inhibition by PCI-34051 attenuates inflammation and airway remodeling in asthmaJournal of translational internal medicine · 2024Article
- Article
- Defective mesenchymal Bmpr1a-mediated BMP signaling causes congenital pulmonary cysts.bioRxiv : the preprint server for biology · 2024Article
- Mesenchymal Stem Extracellular Vesicles in Various Respiratory Diseases: A New Opportunity.Journal of inflammation research · 2024Review
- Article
- Impact of obesity on airway remodeling in asthma: pathophysiological insights and clinical implications.Frontiers in allergy · 2024Review
- Epithelial-Mesenchymal Transition Mechanisms in Chronic Airway Diseases: A Common Process to Target?International journal of molecular sciences · 2023Review
- Long non coding RNAs reveal important pathways in childhood asthma: a future perspective.Journal of molecular histology · 2023Review
- Airway remodeling heterogeneity in asthma and its relationship to disease outcomes.Frontiers in physiology · 2023Review
- Transgenic overexpression of α7 integrin in smooth muscle attenuates allergen-induced airway inflammation in a murine model of asthma.FASEB bioAdvances · 2022Article
- Bronchial smooth muscle cell in asthma: where does it fit?BMJ open respiratory research · 2022Review
- Asthmatic Eosinophils Alter the Gene Expression of Extracellular Matrix Proteins in Airway Smooth Muscle Cells and Pulmonary Fibroblasts.International journal of molecular sciences · 2022Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirway remodeling in asthma is the result of increased expression of connective tissue proteins, airway smooth muscle cell (ASMC) hyperplasia and hypertrophy. TGF-beta1 has been found to increase ASMC proliferation. The activation of mitogen-activated protein kinases (MAPKs), p38, ERK, and JNK, is critical to the signal transduction associated with cell proliferation. In the present study, we determined the role of phosphorylated MAPKs in TGF-beta1 induced ASMC proliferation.
methodsConfluent and growth-arrested bovine ASMCs were treated with TGF-beta1. Proliferation was measured by [3H]-thymidine incorporation and cell counting. Expressions of phosphorylated p38, ERK1/2, and JNK were determined by Western analysis.
resultsIn a concentration-dependent manner, TGF-beta1 increased [3H]-thymidine incorporation and cell number of ASMCs. TGF-beta1 also enhanced serum-induced ASMC proliferation. Although ASMCs cultured with TGF-beta1 had a significant increase in phosphorylated p38, ERK1/2, and JNK, the maximal phosphorylation of each MAPK had a varied onset after incubation with TGF-beta1. TGF-beta1 induced DNA synthesis was inhibited by SB 203580 or PD 98059, selective inhibitors of p38 and MAP kinase kinase (MEK), respectively. Antibodies against EGF, FGF-2, IGF-I, and PDGF did not inhibit the TGF-beta1 induced DNA synthesis.
conclusionOur data indicate that ASMCs proliferate in response to TGF-beta1, which is mediated by phosphorylation of p38 and ERK1/2. These findings suggest that TGF-beta1 which is expressed in airways of asthmatics may contribute to irreversible airway remodeling by enhancing ASMC proliferation.
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Registered trials
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