ArticleThe Journal of biological chemistry2009
Airway epithelial inflammation-induced endoplasmic reticulum Ca2+ store expansion is mediated by X-box binding protein-1.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
- Understanding the impact of ER stress on lung physiology.Frontiers in cell and developmental biology · 2024Review
- IRE1α regulates ROS and immune responses after UVB irradiation.Redox experimental medicine · 2024Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
- Culture with apically applied healthy or disease sputum alters the airway surface liquid proteome and ion transport across human bronchial epithelial cells.American journal of physiology. Cell physiology · 2021Article
- Review
- Copper-Associated Oxidative Stress Contributes to Cellular Inflammatory Responses in Cystic Fibrosis.Biomedicines · 2021Article
- IRE1α Is a Therapeutic Target for Cystic Fibrosis Airway Inflammation.International journal of molecular sciences · 2021Article
- Endoplasmic reticulum stress in human chronic wound healing: Rescue by 4-phenylbutyrate.International wound journal · 2021Article
- The Impact of Endoplasmic Reticulum-Associated Protein Modifications, Folding and Degradation on Lung Structure and Function.Frontiers in physiology · 2021Review
- Airway Epithelial InflammationFrontiers in pharmacology · 2021Article
- Endoplasmic Reticulum Stress-Associated Neuronal Death and Innate Immune Response in Neurological Diseases.Frontiers in immunology · 2021Review
- Lung immunoglobulin A immunity dysregulation in cystic fibrosis.EBioMedicine · 2020Article
- UPR modulation of host immunity by Pseudomonas aeruginosa in cystic fibrosis.Clinical science (London, England : 1979) · 2020Article
- NOD1 and NOD2 Activation by Diverse Stimuli: a Possible Role for Sensing Pathogen-Induced Endoplasmic Reticulum Stress.Infection and immunity · 2020Review
- Review
- Pharmacological modulation of mitochondrial calcium uniporter controls lung inflammation in cystic fibrosis.Science advances · 2020Article
- TNFα selectively activates the IRE1α/XBP1 endoplasmic reticulum stress pathway in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Endoplasmic Reticulum Stress Induces MUC5AC and MUC5B Expression in Human Nasal Airway Epithelial Cells.Clinical and experimental otorhinolaryngology · 2019Article
- The Possible Pathogenesis of Idiopathic Pulmonary Fibrosis consideringBioMed research international · 2019Review
- The cystic fibrosis airway milieu enhances rescue of F508del in a pre-clinical model.The European respiratory journal · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflamed cystic fibrosis (CF) human bronchial epithelia (HBE), or normal HBE exposed to supernatant from mucopurulent material (SMM) from CF airways, exhibit endoplasmic reticulum (ER)/Ca(2+) store expansion and amplified Ca(2+)-mediated inflammation. HBE inflammation triggers an unfolded protein response (UPR) coupled to mRNA splicing of X-box binding protein-1 (XBP-1). Because spliced XBP-1 (XBP-1s) promotes ER expansion in other cellular models, we hypothesized that XBP-1s is responsible for the ER/Ca(2+) store expansion in inflamed HBE. XBP-1s was increased in freshly isolated infected/inflamed CF in comparison with normal HBE. The link between airway epithelial inflammation, XBP-1s, and ER/Ca(2+) store expansion was then addressed in murine airways challenged with phosphate-buffered saline or Pseudomonas aeruginosa. P. aeruginosa-challenged mice exhibited airway epithelial ER/Ca(2+) store expansion, which correlated with airway inflammation. P. aeruginosa-induced airway inflammation triggered XBP-1s in ER stress-activated indicator (ERAI) mice. To evaluate the functional role of XBP-1s in airway inflammation linked to ER/Ca(2+) store expansion, control, XBP-1s, or dominant negative XBP-1 (DN-XBP-1) stably expressing 16HBE14o(-) cell lines were used. Studies with cells transfected with an unfolded protein response element (UPRE) luciferase reporter plasmid confirmed that the UPRE was activated or inhibited by expression of XBP-1s or DN-XBP-1, respectively. Expression of XBP-1s induced ER/Ca(2+) store expansion and potentiated bradykinin-increased interleukin (IL)-8 secretion, whereas expression of DN-XBP-1 inhibited bradykinin-dependent IL-8 secretion. In addition, expression of DN-XBP-1 blunted SMM-induced ER/Ca(2+) store expansion and SMM-induced IL-8 secretion. These findings suggest that, in inflamed HBE, XBP-1s is responsible for the ER/Ca(2+) store expansion that confers amplification of Ca(2+)-dependent inflammatory responses.
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