ArticleAmerican journal of respiratory cell and molecular biology2014
Dysregulation of galectin-3. Implications for Hermansky-Pudlak syndrome pulmonary fibrosis.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Effect of Xinjiang UyghurBioMed research international · 2016Trial
- Chitinase 3-like-1 and its receptors in Hermansky-Pudlak syndrome-associated lung disease.The Journal of clinical investigation · 2015Trial
- Pathophysiology-guided biomarkers and therapeutics for precision trauma medicine in polytrauma with musculoskeletal injuries.Military Medical Research · 2026Review
- Spatial N-glycan rearrangement on αNature communications · 2025Article
- Review
- Anandamide Is a Potential Blood Biomarker of Hermansky-Pudlak Syndrome Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2025Article
- Insights into the renal pathophysiology in Hermansky-Pudlak syndrome-1 from urinary extracellular vesicle proteomics and a new mouse model.FEBS letters · 2025Article
- Impairment of Renal Function in Hermansky-Pudlak Syndrome.American journal of nephrology · 2025Article
- Pathogenesis and Therapy of Hermansky-Pudlak Syndrome (HPS)-Associated Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Review
- Dysregulated myosin in Hermansky-Pudlak syndrome lung fibroblasts is associated with increased cell motility.Respiratory research · 2022Article
- Targeting Chitinase 1 and Chitinase 3-Like 1 as Novel Therapeutic Strategy of Pulmonary Fibrosis.Frontiers in pharmacology · 2022Review
- Modeling of lung phenotype of Hermansky-Pudlak syndrome type I using patient-specific iPSCs.Respiratory research · 2021Article
- CBClinical and translational medicine · 2021Article
- Hermansky-Pudlak syndrome pulmonary fibrosis: a rare inherited interstitial lung disease.European respiratory review : an official journal of the European Respiratory Society · 2021Article
- Automated Digital Quantification of Pulmonary Fibrosis in Human Histopathology Specimens.Frontiers in medicine · 2021Article
- Hermansky-Pudlak Syndrome and Lung Disease: Pathogenesis and Therapeutics.Frontiers in pharmacology · 2021Review
- Bleomycin Induces Drug Efflux in Lungs. A Pitfall for Pharmacological Studies of Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2020Article
- A comprehensive, multidisciplinary, precision medicine approach to discover effective therapy for an undiagnosed, progressive, fibroinflammatory disease.Translational research : the journal of laboratory and clinical medicine · 2020Article
- Idiopathic Pulmonary Fibrosis: New and Emerging Treatment Options.Drugs & aging · 2019Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 1 country.
Funding
Abstract
The etiology of Hermansky-Pudlak syndrome (HPS) pulmonary fibrosis (HPSPF), a progressive interstitial lung disease with high mortality, is unknown. Galectin-3 is a β-galactoside-binding lectin with profibrotic effects. The objective of this study was to investigate the involvement of galectin-3 in HPSPF. Galectin-3 was measured by ELISA, immunohistochemistry, and immunoblotting in human specimens from subjects with HPS and control subjects. Mechanisms of galectin-3 accumulation were studied by quantitative RT-PCR, Northern blot analysis, membrane biotinylation assays, and rescue of HPS1-deficient cells by transfection. Bronchoalveolar lavage galectin-3 concentrations were significantly higher in HPSPF compared with idiopathic pulmonary fibrosis or that from normal volunteers, and correlated with disease severity. Galectin-3 immunostaining was increased in HPSPF compared with idiopathic pulmonary fibrosis or normal lung tissue. Fibroblasts from subjects with HPS subtypes associated with pulmonary fibrosis had increased galectin-3 protein expression compared with cells from nonfibrotic HPS subtypes. Galectin-3 protein accumulation was associated with reduced Galectin-3 mRNA, normal Mucin 1 levels, and up-regulated microRNA-322 in HPSPF cells. Membrane biotinylation assays showed reduced galectin-3 and normal Mucin 1 expression at the plasma membrane in HPSPF cells compared with control cells, which suggests that galectin-3 is mistrafficked in these cells. Reconstitution of HPS1 cDNA into HPS1-deficient cells normalized galectin-3 protein and mRNA levels, as well as corrected galectin-3 trafficking to the membrane. Intracellular galectin-3 levels are regulated by HPS1 protein. Abnormal accumulation of galectin-3 may contribute to the pathogenesis of HPSPF.
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