ArticleRespiratory research2013
Role of Abl in airway hyperresponsiveness and airway remodeling.
Article in Respiratory research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- Article
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- Airway smooth muscle and airway hyperresponsiveness in asthma: mechanisms of airway smooth muscle dysfunction.Minerva medica · 2022Article
- Identification of Signal Pathways and Hub Genes of Pulmonary Arterial Hypertension by Bioinformatic Analysis.Canadian respiratory journal · 2022Article
- Genome-Wide Interaction Study of Late-Onset Asthma With Seven Environmental Factors Using a Structured Linear Mixed Model in Europeans.Frontiers in genetics · 2022Article
- Cooperativity between β-agonists and c-Abl inhibitors in regulating airway smooth muscle relaxation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Integrating Proteomes for Lung Tissues and Lavage Reveals Pathways That Link Responses in Allergen-Challenged Mice.ACS omega · 2021Article
- Ponatinib and other CML Tyrosine Kinase Inhibitors in Thrombosis.International journal of molecular sciences · 2020Review
- Tissue traction microscopy to quantify muscle contraction within precision-cut lung slices.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Inhibiting Airway Smooth Muscle Contraction Using Pitavastatin: A Role for the Mevalonate Pathway in Regulating Cytoskeletal Proteins.Frontiers in pharmacology · 2020Article
- Inhibition of airway remodeling and inflammatory response by Icariin in asthma.BMC complementary and alternative medicine · 2019Article
- Phosphorylation of GMFγ by c-Abl Coordinates Lamellipodial and Focal Adhesion Dynamics to Regulate Airway Smooth Muscle Cell Migration.American journal of respiratory cell and molecular biology · 2019Article
- Orchestrating Airway Smooth Muscle Cell Migration: GMFγ Phosphorylation Is the Key.American journal of respiratory cell and molecular biology · 2019Article
- Plk1 Mediates Paxillin Phosphorylation (Ser-272), Centrosome Maturation, and Airway Smooth Muscle Layer Thickening in Allergic Asthma.Scientific reports · 2019Article
- Reorganization of the Vimentin Network in Smooth Muscle.Journal of engineering and science in medical diagnostics and therapy · 2019Article
- Specific protein 1, c-Abl and ERK1/2 form a regulatory loop.Journal of cell science · 2019Article
- Expression of vitamin D receptor in bronchial asthma and its bioinformatics prediction.Molecular medicine reports · 2018Article
- PDGF-BB regulates the pulmonary vascular tone: impact of prostaglandins, calcium, MAPK- and PI3K/AKT/mTOR signalling and actin polymerisation in pulmonary veins of guinea pigs.Respiratory research · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAsthma is a chronic disease that is characterized by airway hyperresponsiveness and airway remodeling. The underlying mechanisms that mediate the pathological processes are not fully understood. Abl is a non-receptor protein tyrosine kinase that has a role in the regulation of smooth muscle contraction and smooth muscle cell proliferation in vitro. The role of Abl in airway hyperresponsiveness and airway remodeling in vivo is largely unknown.
methodsTo evaluate the role of Abl in asthma pathology, we assessed the expression of Abl in airway tissues from the ovalbumin sensitized and challenged mouse model, and human asthmatic airway smooth muscle cells. In addition, we generated conditional knockout mice in which Abl expression in smooth muscle was disrupted, and then evaluated the effects of Abl conditional knockout on airway resistance, smooth muscle mass, cell proliferation, IL-13 and CCL2 in the mouse model of asthma. Furthermore, we determined the effects of the Abl pharmacological inhibitors imatinib and GNF-5 on these processes in the animal model of asthma.
resultsThe expression of Abl was upregulated in airway tissues of the animal model of asthma and in airway smooth muscle cells of patients with severe asthma. Conditional knockout of Abl attenuated airway resistance, smooth muscle mass and staining of proliferating cell nuclear antigen in the airway of mice sensitized and challenged with ovalbumin. Interestingly, conditional knockout of Abl did not affect the levels of IL-13 and CCL2 in bronchoalveolar lavage fluid of animals treated with ovalbumin. However, treatment with imatinib and GNF-5 inhibited the ovalbumin-induced increase in IL-13 and CCL2 as well as airway resistance and smooth muscle growth in animals.
conclusionsThese results suggest that the altered expression of Abl in airway smooth muscle may play a critical role in the development of airway hyperresponsiveness and airway remodeling in asthma. Our findings support the concept that Abl may be a novel target for the development of new therapy to treat asthma.
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