ArticleThe Journal of biological chemistry2010
The chitinase-like protein YKL-40 is secreted by airway epithelial cells at base line and in response to compressive mechanical stress.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.
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Who cites it
49 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- A molecular systems architecture of asthma.Frontiers in immunology · 2026Pooled it
- Association between risk of asthma and gene polymorphisms in CHI3L1 and CHIA: a systematic meta-analysis.BMC pulmonary medicine · 2017Pooled it
- Concurrent jamming and mesenchymal-to-epithelial transitions during airway basal stem cell differentiation.iScience · 2026Article
- Mechanically induced dysregulation of calcium homeostasis: a molecular linchpin in asthmatic pathogenesis.European journal of medical research · 2025Review
- Hic-5 drives epithelial mechanotransduction promoting a feed-forward cycle of bronchoconstriction.Nature communications · 2025Article
- TGF-β Receptor-dependent Tissue Factor Release and Proteomic Profiling of Extracellular Vesicles from Mechanically Compressed Human Bronchial Epithelial Cells.American journal of respiratory cell and molecular biology · 2025Article
- Multimodal single-cell analyses reveal mechanisms of perianal fistula in diverse patients with Crohn's disease.Med (New York, N.Y.) · 2024Article
- The Role of Chitinase-3-like Protein-1 (YKL40) in the Therapy of Cancer and Other Chronic-Inflammation-Related Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Immunologic aspects of asthma: from molecular mechanisms to disease pathophysiology and clinical translation.Frontiers in immunology · 2024Review
- Mechanical forces suppress antiviral innate immune responses from asthmatic airway epithelial cells following rhinovirus infection.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Quantification of basal stem cell elongation and stress fiber accumulation in the pseudostratified airway epithelium during the unjamming transition.Biology open · 2023Article
- CRTH2 in Pulmonary Fibrosis: Friend or Foe?American journal of respiratory cell and molecular biology · 2022Article
- Article
- Reciprocal induction of hepatitis C virus replication and stimulation of hepatic profibrogenic cytokine release and cellular viability by YKL-40.Annals of translational medicine · 2021Article
- Genomic signatures of the unjamming transition in compressed human bronchial epithelial cells.Science advances · 2021Article
- Bronchoconstriction: a potential missing link in airway remodelling.Open biology · 2020Review
- In primary airway epithelial cells, the unjamming transition is distinct from the epithelial-to-mesenchymal transition.Nature communications · 2020Article
- Airway mechanical compression: its role in asthma pathogenesis and progression.European respiratory review : an official journal of the European Respiratory Society · 2020Review
- Article
- [Changes in serum human cartilage glycoprotein-39 and high-mobility group box 1 in preterm infants with bronchopulmonary dysplasia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The chitinase-like protein YKL-40, encoded by the CHI3L1 gene, is a biomarker and functional effector of chronic inflammatory and allergic diseases. In the lung it is associated with asthma severity and reduced lung function. The cellular sources of YKL-40 in human airways and the mechanisms regulating YKL-40 expression are poorly understood. We previously showed that mechanical stress similar to that experienced during bronchoconstriction triggers epithelial cell signaling through epidermal growth factor receptor (EGFR), fibrotic mediator release, and goblet cell hyperplasia consistent with airway remodeling in asthma. We now show that well differentiated normal human bronchial epithelial cells express CHI3L1 and secrete YKL-40 under base-line culture conditions. Mechanical stress (30-cm H(2)O transcellular compressive stress) applied for 3 h induces CHI3L1 expression by ∼4-fold compared with time matched controls, resulting in increased secretion of YKL-40 by 3.6-fold 24 h after onset of the 3-h stimulus. Inhibition of EGFR or MEK1/2 (ERK kinase) significantly but incompletely attenuates mechanical stress-induced up-regulation of CHI3L1 expression in normal human bronchial epithelial cells. Direct activation of EGFR utilizing EGF-family ligands induces CHI3L1 expression. Our results reveal that human airway epithelial cells are a source of YKL-40 and demonstrate that mechanical stress potently induces CHI3L1 expression leading to increased secretion of YKL-40 protein in an EGFR and MEK1/2-dependent pathway. In the asthmatic airway mechanical stress may contribute to enhanced YKL-40 levels.
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