ArticleRespiratory research2015
Tight junction disruption by cadmium in an in vitro human airway tissue model.
Article in Respiratory research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Toxic metal exposure as a possible risk factor for COVID-19 and other respiratory infectious diseases.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020Pooled it
- The Role of the Gut-Liver Axis in the Development of Liver Diseases Induced by Selected Environmental Pollutants: A Narrative Review.International journal of molecular sciences · 2026Review
- Breathing lung-on-chip: a versatile tool for assessing respiratory toxicity across multiple therapeutic modalities.Archives of toxicology · 2026Article
- Cadmium-induced DAG-PKC/IP3-Ca2+ double signaling pathway and cell injury in gill of freshwater crabs Sinopotamon henanense.PloS one · 2026Article
- Association between heavy metal exposure and chronic cough: the mediating roles of inflammation.Annals of medicine · 2025Article
- Cadmium Induces Vascular Endothelial Cell Detachment by Downregulating Claudin-5 and ZO-1 Levels.International journal of molecular sciences · 2024Article
- Heavy Metal Exposure-Mediated Dysregulation of Sphingolipid Metabolism.Antioxidants (Basel, Switzerland) · 2024Article
- Low dose cadmium exposure regulates miR-381-ANO1 interaction in airway epithelial cells.Scientific reports · 2024Article
- Occludin: a gatekeeper of brain Infection by HIV-1.Fluids and barriers of the CNS · 2023Review
- Parallel evaluation of alternative skin barrier models and excised human skin for dermal absorption studies in vitro.Toxicology in vitro : an international journal published in association with BIBRA · 2023Article
- Development of a micronucleus test using the EpiAirway™ organotypic human airway model.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- Disease-associated metabolic pathways affected by heavy metals and metalloid.Toxicology reports · 2023Review
- Effects of SPA4 peptide on lipopolysaccharide-disrupted lung epithelial barrier, injury, and function in a human cell system and mouse model of lung injury.Physiological reports · 2022Article
- Environmental Factors Influencing COVID-19 Incidence and Severity.Annual review of public health · 2022Review
- The Role of Defective Epithelial Barriers in Allergic Lung Disease and Asthma Development.Journal of asthma and allergy · 2022Review
- Small-molecule Akt-activation in airway cells induces NO production and reduces IL-8 transcription through Nrf-2.Respiratory research · 2021Article
- Electronic cigarette smoke reduces ribosomal protein gene expression to impair protein synthesis in primary human airway epithelial cells.Scientific reports · 2021Article
- The Relationship between the Urinary Cadmium Concentration and Cause-Specific Mortality in Subjects without Severe Renal Damage: A 35-Year Follow-Up Study in a Cadmium-Polluted Area of Japan.International journal of environmental research and public health · 2021Article
- Genetic toxicity testing using human in vitro organotypic airway cultures: Assessing DNA damage with the CometChip and mutagenesis by Duplex Sequencing.Environmental and molecular mutagenesis · 2021Article
- PAR-2-activated secretion by airway gland serous cells: role for CFTR and inhibition byAmerican journal of physiology. Lung cellular and molecular physiology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe cadmium (Cd) present in air pollutants and cigarette smoke has the potential of causing multiple adverse health outcomes involving damage to pulmonary and cardiovascular tissue. Injury to pulmonary epithelium may include alterations in tight junction (TJ) integrity, resulting in impaired epithelial barrier function and enhanced penetration of chemicals and biomolecules. Herein, we investigated mechanisms involved in the disruption of TJ integrity by Cd exposure using an in vitro human air-liquid-interface (ALI) airway tissue model derived from normal primary human bronchial epithelial cells.
methodsALI cultures were exposed to noncytotoxic doses of CdCl2 basolaterally and TJ integrity was measured by Trans-Epithelial Electrical Resistance (TEER) and immunofluorescence staining with TJ markers. PCR array analysis was used to identify genes involved with TJ collapse. To explore the involvement of kinase signaling pathways, cultures were treated with CdCl2 in the presence of kinase inhibitors specific for cellular Src or Protein Kinase C (PKC).
resultsNoncytotoxic doses of CdCl2 resulted in the collapse of barrier function, as demonstrated by TEER measurements and Zonula occludens-1 (ZO-1) and occludin staining. CdCl2 exposure altered the expression of several groups of genes encoding proteins involved in TJ homeostasis. In particular, down-regulation of select junction-interacting proteins suggested that a possible mechanism for Cd toxicity involves disruption of the peripheral junctional complexes implicated in connecting membrane-bound TJ components to the actin cytoskeleton. Inhibition of kinase signaling using inhibitors specific for cellular Src or PKC preserved the integrity of TJs, possibly by preventing occludin tyrosine hyperphosphorylation, rather than reversing the down-regulation of the junction-interacting proteins.
conclusionsOur findings indicate that acute doses of Cd likely disrupt TJ integrity in human ALI airway cultures both through occludin hyperphosphorylation via kinase activation and by direct disruption of the junction-interacting complex.
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