ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Elevated expression of NEU1 sialidase in idiopathic pulmonary fibrosis provokes pulmonary collagen deposition, lymphocytosis, and fibrosis.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mammalian Neuraminidases in Immune-Mediated Diseases: Mucins and Beyond.Frontiers in immunology · 2022Pooled it
- Endothelial glycosylation and its emerging role in pulmonary vascular health and disease.Nature communications · 2025Review
- Mechanistic and Therapeutic Implications of Protein and Lipid Sialylation in Human Diseases.International journal of molecular sciences · 2024Review
- Neuraminidase-1 (NEU1): Biological Roles and Therapeutic Relevance in Human Disease.Current issues in molecular biology · 2024Review
- The role of sialidase Neu1 in respiratory diseases.Respiratory research · 2024Review
- Metabolism-driven glycosylation represents therapeutic opportunities in interstitial lung diseases.Frontiers in immunology · 2024Review
- Neuraminidase 1 promotes renal fibrosis development in male mice.Nature communications · 2023Article
- Targeting protein glycosylation to regulate inflammation in the respiratory tract: novel diagnostic and therapeutic candidates for chronic respiratory diseases.Frontiers in immunology · 2023Review
- Full-length IL-33 augments pulmonary fibrosis in an ST2- and Th2-independent, non-transcriptomic fashion.Cellular immunology · 2023Article
- Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022Review
- The extracellular sialidase NEU3 primes neutrophils.Journal of leukocyte biology · 2022Article
- Sialidase Inhibitors with Different Mechanisms.Journal of medicinal chemistry · 2022Review
- The sialidase NEU3 promotes pulmonary fibrosis in mice.Respiratory research · 2022Article
- Altered sialidase expression in human myeloid cells undergoing apoptosis and differentiation.Scientific reports · 2022Article
- Inhibitors of Human Neuraminidase Enzymes Block TransmigrationFrontiers in molecular biosciences · 2022Article
- Discovery of NEU1 as a candidatedone. renal biomarker for proliferative lupus nephritis chronicity.Lupus science & medicine · 2021Article
- Influenza Virus Infects and Depletes Activated Adaptive Immune Responders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Therapeutic Effect of Neuraminidase-1-Selective Inhibition in Mouse Models of Bleomycin-Induced Pulmonary Inflammation and Fibrosis.The Journal of pharmacology and experimental therapeutics · 2021Article
- Serum Amyloid P inhibits single stranded RNA-induced lung inflammation, lung damage, and cytokine storm in mice.PloS one · 2021Article
- Inhibiting Sialidase-Induced TGF-The Journal of pharmacology and experimental therapeutics · 2021Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) poses challenges to understanding its underlying cellular and molecular mechanisms and the development of better therapies. Previous studies suggest a pathophysiological role for neuraminidase 1 (NEU1), an enzyme that removes terminal sialic acid from glycoproteins. We observed increased NEU1 expression in epithelial and endothelial cells, as well as fibroblasts, in the lungs of patients with IPF compared with healthy control lungs. Recombinant adenovirus-mediated gene delivery of NEU1 to cultured primary human cells elicited profound changes in cellular phenotypes. Small airway epithelial cell migration was impaired in wounding assays, whereas, in pulmonary microvascular endothelial cells, NEU1 overexpression strongly impacted global gene expression, increased T cell adhesion to endothelial monolayers, and disrupted endothelial capillary-like tube formation. NEU1 overexpression in fibroblasts provoked increased levels of collagen types I and III, substantial changes in global gene expression, and accelerated degradation of matrix metalloproteinase-14. Intratracheal instillation of NEU1 encoding, but not control adenovirus, induced lymphocyte accumulation in bronchoalveolar lavage samples and lung tissues and elevations of pulmonary transforming growth factor-β and collagen. The lymphocytes were predominantly T cells, with CD8(+) cells exceeding CD4(+) cells by nearly twofold. These combined data indicate that elevated NEU1 expression alters functional activities of distinct lung cell types in vitro and recapitulates lymphocytic infiltration and collagen accumulation in vivo, consistent with mechanisms implicated in lung fibrosis.
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