ArticleAnnals of the New York Academy of Sciences2020
Acute cytotoxicity and increased vascular endothelial growth factor after in vitro nitrogen mustard vapor exposure.
Article in Annals of the New York Academy of Sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Comprehensive reexamination of the acute toxicity of nitrogen mustards: HN-1, HN-2 and HN-3 as blister agents: application of multi in silico approach.Archives of toxicology · 2025Article
- Single-cell resolution of human airway epithelial cells exposed to bronchiolitis obliterans-associated chemicals.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Eruptive Cherry Angiomas After Nitrogen Mustard Treatment for Vitiligo.Clinical, cosmetic and investigational dermatology · 2024Article
- Heterogeneity in Neutrophil Extracellular Traps from Healthy Human Subjects.International journal of molecular sciences · 2023Article
- Heterogeneity in Neutrophil Extracellular Traps from Healthy Human Subjects.bioRxiv : the preprint server for biology · 2023Article
- Vascular Inflammation, Cancer, and Cardiovascular Diseases.Current oncology reports · 2023Review
- Alpha-1 antitrypsin limits neutrophil extracellular trap disruption of airway epithelial barrier function.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Nitrogen mustard (NM) is a highly toxic alkylating agent. Inhalation exposure can cause acute and chronic lung injury. This study's aims were to develop an in vitro coculture model of mustard-induced airway injury and to identify growth factors contributing to airway pathology. Primary human bronchial epithelial cells cultured with pulmonary endothelial cells were exposed to NM (25, 50, 100, 250, or 500 μM) or PBS (control) for 1 hour. Lactate dehydrogenase (LDH) and transepithelial electrical resistance (TEER) were measured before and 24 h after NM exposure. Fixed cultures were stained for hematoxylin and eosin or live/dead staining. Culture media were analyzed for 11 growth factors. A 1-h vapor exposure to greater than or equal to 50 μM NM increased supernatant LDH, decreased TEER, and caused airway epithelial cell detachment. Endothelial cell death occurred at 500 μM NM. Vascular endothelial growth factor A (VEGF-A) and placental growth factor (PlGF) expression increased in 500 μM NM-exposed cultures compared with PBS-exposed control cultures. NM vapor exposure causes differential cytotoxicity to airway epithelial and endothelial injury in culture. Increased VEGF-A and PlGF expression occurred acutely in airway cocultures. Future studies are required to validate the role of VEGF signaling in mustard-induced airway pathology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.