ArticleAmerican journal of physiology. Lung cellular and molecular physiology2009
Insulin receptor substrate-1/2 mediates IL-4-induced migration of human airway epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Type 2 inflammation drives an airway basal stem cell program through insulin receptor substrate signaling.The Journal of allergy and clinical immunology · 2023Article
- The Role of Insulin Receptor Substrate Proteins in Bronchopulmonary Dysplasia and Asthma: New Potential Perspectives.International journal of molecular sciences · 2022Review
- Genome-wide DNA methylation analysis of pulmonary function in middle and old-aged Chinese monozygotic twins.Respiratory research · 2021Article
- Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases.BioMed research international · 2018Review
- New insights into the mechanisms of pulmonary edema in acute lung injury.Annals of translational medicine · 2018Review
- Chemokine expression in the early response to injury in human airway epithelial cells.PloS one · 2018Article
- Amnion Epithelial Cells Promote Lung Repair via Lipoxin AStem cells translational medicine · 2017Article
- Peripheral blood IRF1 expression as a marker for glucocorticoid sensitivity.Pharmacogenetics and genomics · 2015Article
- Regulation of macrophage motility by the water channel aquaporin-1: crucial role of M0/M2 phenotype switch.PloS one · 2015Article
- Delay of airway epithelial wound repair in COPD is associated with airflow obstruction severity.Respiratory research · 2014Article
- Article
- Human leukocyte antigen-G expression in differentiated human airway epithelial cells: lack of modulation by Th2-associated cytokines.Respiratory research · 2013Article
- Knowledge translation: airway epithelial cell migration and respiratory diseases.Cellular and molecular life sciences : CMLS · 2012Review
- Acute lung injury: how macrophages orchestrate resolution of inflammation and tissue repair.Frontiers in immunology · 2011Article
- Expression of IL-4/IL-13 receptors in differentiating human airway epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- Epithelial repair mechanisms in the lung.American journal of physiology. Lung cellular and molecular physiology · 2010Review
- The signaling adaptor insulin receptor substrate 2 (IRS2) limits lethal host responses induced by influenza infection.Innate immunityArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Migration of airway epithelial cells (AEC) is an integral component of airway mucosal repair after injury. The inflammatory cytokine IL-4, abundant in chronic inflammatory airways diseases such as asthma, stimulates overproduction of mucins and secretion of chemokines from AEC; these actions enhance persistent airway inflammation. The effect of IL-4 on AEC migration and repair after injury, however, is not known. We examined migration in primary human AEC differentiated in air-liquid interface culture for 3 wk. Wounds were created by mechanical abrasion and followed to closure using digital microscopy. Concurrent treatment with IL-4 up to 10 ng/ml accelerated migration significantly in fully differentiated AEC. As expected, IL-4 treatment induced phosphorylation of the IL-4 receptor-associated protein STAT (signal transducer and activator of transcription)6, a transcription factor known to mediate several IL-4-induced AEC responses. Expressing a dominant negative STAT6 cDNA delivered by lentivirus infection, however, failed to block IL-4-stimulated migration. In contrast, decreasing expression of either insulin receptor substrate (IRS)-1 or IRS-2 using a silencing hairpin RNA blocked IL-4-stimulated AEC migration completely. These data demonstrate that IL-4 can accelerate migration of differentiated AEC after injury. This reparative response does not require STAT6 activation, but rather requires IRS-1 and/or IRS-2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.