ArticleAmerican journal of respiratory and critical care medicine2010
The chitinase-like proteins breast regression protein-39 and YKL-40 regulate hyperoxia-induced acute lung injury.
Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 114 citations in OpenAlex.
- Chitinase 3-like-1 and its receptors in Hermansky-Pudlak syndrome-associated lung disease.The Journal of clinical investigation · 2015Trial
- Kasugamycin Inhibits Melanoma Lung Metastasis and CHI3L1-Driven M2-Like Tumor-Associated Macrophage Differentiation.ImmunoTargets and therapy · 2026Article
- Up-regulated chitinase-like protein-1 promotes tumour growth while physiological levels are protective.Life science alliance · 2025Article
- Generation of a Ym1 deficient mouse utilising CRISPR-Cas9 in CB6 embryos.Transgenic research · 2025Article
- Article
- Aberrant Chitinase 3-Like 1 Expression in Basal Cells Contributes to Systemic Sclerosis Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inhibition of BRD4 activates the AKT-SIRT3 signaling pathway to suppress apoptosis and attenuate hyperoxia-induced lung injury.Frontiers in bioengineering and biotechnology · 2025Article
- Inflammatory Effects and Regulatory Mechanisms of Chitinase-3-like-1 in Multiple Human Body Systems: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Type 2 innate immunity promotes the development of pulmonary fibrosis in Hermansky-Pudlak syndrome.JCI insight · 2024Article
- Chitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Chitinase 3-like-1 (CHI3L1) in the pathogenesis of epidermal growth factor receptor mutant non-small cell lung cancer.Translational oncology · 2024Article
- Inconsequential role for chemerin-like receptor 1 in the manifestation of ozone-induced lung pathophysiology in male mice.Physiological reports · 2024Article
- Combined gestational age and serum fucose for early prediction of risk for bronchopulmonary dysplasia in premature infants.BMC pediatrics · 2024Article
- Location-based prediction model for Crohn's disease regarding a novel serological marker, anti-chitinase 3-like 1 autoantibodies.World journal of gastroenterology · 2023Article
- NLRX1 knockdown attenuates pro-apoptotic signaling and cell death in pulmonary hyperoxic acute injury.Scientific reports · 2023Article
- Chitinase 3 like 1 contributes to the development of pulmonary vascular remodeling in pulmonary hypertension.JCI insight · 2022Article
- CRTH2 Mediates Profibrotic Macrophage Differentiation and Promotes Lung Fibrosis.American journal of respiratory cell and molecular biology · 2022Article
- Urine Proteomics for Noninvasive Monitoring of Biomarkers in Bronchopulmonary Dysplasia.Neonatology · 2022Article
- Targeting Chitinase 1 and Chitinase 3-Like 1 as Novel Therapeutic Strategy of Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- CHI3L1 enhances melanoma lung metastasisFrontiers in immunology · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
rationaleProlonged exposure to 100% O(2) causes hyperoxic acute lung injury (HALI), characterized by alveolar epithelial cell injury and death. We previously demonstrated that the murine chitinase-like protein, breast regression protein (BRP)-39 and its human homolog, YKL-40, inhibit cellular apoptosis. However, the regulation and roles of these molecules in hyperoxia have not been addressed.
objectivesWe hypothesized that BRP-39 and YKL-40 (also called chitinase-3-like 1) play important roles in the pathogenesis of HALI.
methodsWe characterized the regulation of BRP-39 during HALI and the responses induced by hyperoxia in wild-type mice, BRP-39-null (-/-) mice, and BRP-39(-/-) mice in which YKL-40 was overexpressed in respiratory epithelium. We also compared the levels of tracheal aspirate YKL-40 in premature newborns with respiratory failure. MEASUREMENTS AND MAIN
resultsThese studies demonstrate that hyperoxia inhibits BRP-39 in vivo in the murine lung and in vitro in epithelial cells. They also demonstrate that BRP-39(-/-) mice have exaggerated permeability, protein leak, oxidation, inflammatory, chemokine, and epithelial apoptosis responses, and experience premature death in 100% O(2). Lastly, they demonstrate that YKL-40 ameliorates HALI, prolongs survival in 100% O(2), and rescues the exaggerated injury response in BRP-39(-/-) animals. In accord with these findings, the levels of tracheal aspirate YKL-40 were lower in premature infants treated with hyperoxia for respiratory failure who subsequently experienced bronchopulmonary dysplasia or death compared with those that did not experience these complications.
conclusionsThese studies demonstrate that hyperoxia inhibits BRP-39/YKL-40, and that BRP-39 and YKL-40 are critical regulators of oxidant injury, inflammation, and epithelial apoptosis in the murine and human lung.
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Registered trials
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