ArticleRespiratory research2017
The role of Src & ERK1/2 kinases in inspiratory resistive breathing induced acute lung injury and inflammation.
Article in Respiratory research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- An update on regulation of the polymodal TRPV4 channel by protein phosphorylation.Channels (Austin, Tex.) · 2026Review
- 6β-Acetoxysandaracopimaradien-1α,9α-diol Attenuates LPS-Induced Acute Lung Injury: Association with Alterations in Src, MAPK, and Akt/GSK-3β Signalling.International journal of molecular sciences · 2026Article
- Major pathophysiological changes in pulmonary disease provided a molecular insight based on deep learning approach.Scientific reports · 2025Article
- Resistive breathing aggravates cigarette smoke-induced pulmonary inflammation.ERJ open research · 2025Article
- Resistive spontaneous breathing exacerbated lipopolysaccharide-induced lung injury in mice.Biochemistry and biophysics reports · 2024Article
- The Na/K-ATPase role as a signal transducer in lung inflammation.Frontiers in immunology · 2023Review
- Network Pharmacology and Experimental Validation to Explore the Mechanism of Qing-Jin-Hua-Tan-Decoction Against Acute Lung Injury.Frontiers in pharmacology · 2022Article
- Proto-oncogene tyrosine-protein kinase SRC (Src) inhibition in microglia relieves neuroinflammation in neuropathic pain mouse models.Bioengineered · 2021Article
- Ginkgolide C attenuates lipopolysaccharide‑induced acute lung injury by inhibiting inflammation via regulating the CD40/NF‑κB signaling pathway.International journal of molecular medicine · 2021Article
- Bioinformatics analysis of the potential biomarkers for acute respiratory distress syndrome.Bioscience reports · 2020Article
- p38 Inhibition Ameliorates Inspiratory Resistive Breathing-Induced Pulmonary Inflammation.Inflammation · 2018Article
- The ERK/CREB pathway is involved in the c-Ski expression induced by low TGF-β1 concentrations during primary fibroblast proliferation.Cell cycle (Georgetown, Tex.) · 2018Article
- TRPV4 Inhibition Exerts Protective Effects Against Resistive Breathing Induced Lung Injury.International journal of chronic obstructive pulmonary diseaseArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInspiratory resistive breathing (IRB), a hallmark of obstructive airway diseases, is associated with large negative intrathoracic pressures, due to strenuous contractions of the inspiratory muscles. IRB is shown to induce lung injury in previously healthy animals. Src is a multifunctional kinase that is activated in the lung by mechanical stress. ERK1/2 kinase is a downstream target of Src. We hypothesized that Src is activated in the lung during IRB, mediates ERK1/2 activation and IRB-induced lung injury.
methodsAnaesthetized, tracheostomized adult rats breathed spontaneously through a 2-way non-rebreathing valve. Resistance was added to the inspiratory port to provide a peak tidal inspiratory pressure of 50% of maximum (inspiratory resistive breathing). Activation of Src and ERK1/2 in the lung was estimated during IRB. Following 6 h of IRB, respiratory system mechanics were measured by the forced oscillation technique and bronchoalveolar lavage (BAL) was performed to measure total and differential cell count and total protein levels. IL-1b and MIP-2a protein levels were measured in lung tissue samples. Wet lung weight to total body weight was measured and Evans blue dye extravasation was estimated to measure lung permeability. Lung injury was evaluated by histology. The Src inhibitor, PP-2 or the inhibitor of ERK1/2 activation, PD98059 was administrated 30 min prior to IRB.
resultsSrc kinase was activated 30 min after the initiation of IRB. Src inhibition ameliorated the increase in BAL cellularity after 6 h IRB, but not the increase of IL-1β and MIP-2a in the lung. The increase in BAL total protein and lung injury score were not affected. The increase in tissue elasticity was partly inhibited. Src inhibition blocked ERK1/2 activation at 3 but not at 6 h of IRB. ERK1/2 inhibition ameliorated the increase in BAL cellularity after 6 h of IRB, blocked the increase of IL-1β and returned Evans blue extravasation and wet lung weight to control values. BAL total protein and the increase in elasticity were partially affected. ERK1/2 inhibition did not significantly change total lung injury score compared to 6 h IRB.
conclusionsSrc and ERK1/2 are activated in the lung following IRB and participate in IRB-induced lung injury.
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