ArticleAmerican journal of respiratory cell and molecular biology2006
The role of metallothionein in the pathogenesis of acute lung injury.
Article in American journal of respiratory cell and molecular biology, 2006. 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.
- Article
- A proteomics and redox proteomics approach to understanding ARDS heterogeneity.Scientific reports · 2026Article
- Single cell transcriptomics in a treatment-segregated cohort exposes a STAT3-regulated therapeutic gap in idiopathic pulmonary fibrosis.bioRxiv : the preprint server for biology · 2025Article
- Cardiopulmonary bypass with deep hypothermic circulatory arrest results in organ-specific transcriptomic responses in pediatric swine.Translational research : the journal of laboratory and clinical medicine · 2025Article
- Alveolar macrophages in lung cancer: opportunities challenges.Frontiers in immunology · 2023Review
- Exacerbation of Elastase-Induced Emphysema via Increased Oxidative Stress in Metallothionein-Knockout Mice.Biomolecules · 2022Article
- Characterization of the COPD alveolar niche using single-cell RNA sequencing.Nature communications · 2022Article
- Article
- Zinc deficiency primes the lung for ventilator-induced injury.JCI insight · 2017Article
- Zerovalent Fe, Co and Ni nanoparticle toxicity evaluated on SKOV-3 and U87 cell lines.Journal of applied toxicology : JAT · 2016Article
- Proteomic Assessment of Biochemical Pathways That Are Critical to Nickel-Induced Toxicity Responses in Human Epithelial Cells.PloS one · 2016Article
- Molecular signatures in the prevention of radiation damage by the synergistic effect of N-acetyl cysteine and qingre liyan decoction, a traditional chinese medicine, using a 3-dimensional cell culture model of oral mucositis.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- EOLA1 protects lipopolysaccharide induced IL-6 production and apoptosis by regulation of MT2A in human umbilical vein endothelial cells.Molecular and cellular biochemistry · 2014Article
- Zinc and the prooxidant heart failure phenotype.Journal of cardiovascular pharmacology · 2014Review
- Gene expression profiles analysis identifies key genes for acute lung injury in patients with sepsis.Diagnostic pathology · 2014Article
- Metallothionein and stress combine to affect multiple organ systems.Cell stress & chaperones · 2014Review
- Efficacy of AiiM, an N-acylhomoserine lactonase, against Pseudomonas aeruginosa in a mouse model of acute pneumonia.Antimicrobial agents and chemotherapy · 2013Article
- Metallothionein-induced zinc partitioning exacerbates hyperoxic acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Article
- Haplotype association mapping of acute lung injury in mice implicates activin a receptor, type 1.American journal of respiratory and critical care medicine · 2011Article
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Authors and funding
12 authors.
Funding
Abstract
Often fatal, acute lung injury has a complicated etiology. Previous studies from our laboratory in mice have demonstrated that survival during acute lung injury is a complex trait governed by multiple loci. We also found that the increase in metallothionein (MT) is one of the greatest noted in transcriptome-wide analyses of gene expression. To assess the role of MT in nickel-induced acute lung injury, the survival of Mt-transgenic, Mt1/2(+/+), and Mt1/2(-/-) mice was compared. Pulmonary inflammation and global gene expression were compared in Mt1/2(+/+) and Mt1/2(-/-) mice. Gene-targeted Mt1/2(-/-) mice were more susceptible than Mt1/2(+/+) mice to nickel-induced inflammation, surfactant-associated protein B transcript loss, and lethality. Similarly, Mt-transgenic mice exhibited increased survival. MAPPFinder analyses also noted significant decreases in genes involved in protein processing (e.g., ubiquitination, folding), which were greater in Mt1/2(-/-) mice as compared with Mt1/2(+/+) mice early in the progression of acute lung injury, possibly due to a zinc-mediated transcript destabilization. In contrast, transcript levels of genes associated with the inflammatory response, extracellular matrix regulation, and coagulation/fibrinolysis were increased more in Mt1/2(-/-) mice as compared with Mt1/2(+/+) mice late in the development of acute lung injury. Thus, MT ultimately improves survival in the progression of acute lung injury in mice. Transcriptome-wide analysis suggests that this survival may be mediated through changes in the destabilization of transcripts associated with protein processing, the subsequent augmentation of transcripts controlling inflammation, extracellular matrix regulation, coagulation/fibrinolysis, and disruption of surfactant homeostasis.
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