ArticleScientific reports2021
Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Extracellular Vesicles and Endocrine Disruption: How Environmental Pollutants Modulate the Loading and Release of Extracellular Vesicles for Cancer Promotion and Progression.International journal of molecular sciences · 2026Review
- Article
- Extracellular vesicle-encapsulated microRNA signatures of cigarette smoking and smoking-related harm.Respiratory medicine · 2025Article
- Airway basal stem cell-derived extracellular vesicles modulate proliferation, migration and collagen deposition of fibroblasts.Stem cell research & therapy · 2025Article
- Effectiveness of extracellular vesicles derived from hiPSCs in repairing hyperoxia-induced injury in a fetal murine lung explant model.Stem cell research & therapy · 2024Article
- Exploring salivary exosomes as early predictors of oral cancer in susceptible tobacco consumers: noninvasive diagnostic and prognostic applications.Journal of cancer research and clinical oncology · 2023Article
- Expression and correlation of the Pi3k/Akt pathway and VEGF in oral submucous fibrosis.Cell proliferation · 2023Article
- Initial and ongoing tobacco smoking elicits vascular damage and distinct inflammatory response linked to neurodegeneration.Brain, behavior, & immunity - health · 2023Article
- Extracellular Vesicles (EVs) as Crucial Mediators of Cell-Cell Interaction in Asthma.International journal of molecular sciences · 2023Review
- Do Circulating Extracellular Vesicles Strictly Reflect Bronchoalveolar Lavage Extracellular Vesicles in COPD?International journal of molecular sciences · 2023Article
- Hesperidin inhibits tobacco smoke-induced pulmonary cell proliferation and EMT in mouse lung tissues via the p38 signaling pathway.Oncology letters · 2023Article
- The impact of environmental contaminants on extracellular vesicles and their key molecular regulators: A literature and database-driven review.Environmental and molecular mutagenesis · 2023Review
- Environmental Exposures and Extracellular Vesicles: Indicators of Systemic Effects and Human Disease.Current environmental health reports · 2022Review
- Endothelial Dysfunction through Oxidatively Generated Epigenetic Mark in Respiratory Viral Infections.Cells · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The human airway epithelium lining the bronchial tree contains basal cells that proliferate, differentiate, and communicate with other components of their microenvironment. One method that cells use for intercellular communication involves the secretion of exosomes and other extracellular vesicles (EVs). We isolated exosome-enriched EVs that were produced from an immortalized human airway basal cell line (BCi-NS1.1) and found that their secretion is increased by exposure to cigarette smoke extract, suggesting that this stress stimulates release of EVs which could affect signaling to other cells. We have previously shown that primary human airway basal cells secrete vascular endothelial growth factor A (VEGFA) which can activate MAPK signaling cascades in endothelial cells via VEGF receptor-2 (VEGFR2). Here, we show that exposure of endothelial cells to exosome-enriched airway basal cell EVs promotes the survival of these cells and that this effect also involves VEGFR2 activation and is, at least in part, mediated by VEGFA present in the EVs. These observations demonstrate that EVs are involved in the intercellular signaling between airway basal cells and the endothelium which we previously reported. The downstream signaling pathways involved may be distinct and specific to the EVs, however, as increased phosphorylation of Akt, STAT3, p44/42 MAPK, and p38 MAPK was not seen following exposure of endothelial cells to airway basal cell EVs.
Indexed as
Identifiers
What OpenQuestion holds
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.