ArticleAmerican journal of respiratory cell and molecular biology2014
Smoking exposure induces human lung endothelial cell adaptation to apoptotic stress.
Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04918706 (An Explorative Study for Halting Inflammation in Patients With Emphysema by Administration of Allogeneic Bone Marrow Derived Mesenchymal Stromal Cells.), which is not on this map. Cited by 33 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.
An Explorative Study for Halting Inflammation in Patients With Emphysema by Administration of Allogeneic Bone Marrow Derived Mesenchymal Stromal Cells.
Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- Modelling cigarette smoke-induced lung vascular dysfunction using an alveolus-on-chip.Materials today. Bio · 2026Article
- Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions.The Journal of pathology · 2026Review
- Short-Term Acid Sphingomyelinase Deficiency Exerts Proinflammatory and Antiapoptotic Effects during LPS-induced Lung Injury in Mice.American journal of respiratory cell and molecular biology · 2025Article
- Exploring hypoxia driven subtypes of pulmonary arterial hypertension through transcriptomics single cell sequencing and machine learning.Scientific reports · 2025Article
- Extracellular vesicular delivery of ceramides from pulmonary macrophages to endothelial cells facilitates chronic obstructive pulmonary disease.Cell communication and signaling : CCS · 2025Article
- Does Chronic Obstructive Pulmonary Disease Originate from Different Cell Types?American journal of respiratory cell and molecular biology · 2023Article
- Ceramide as an endothelial cell surface receptor and a lung-specific lipid vascular target for circulating ligands.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Marked elevations in lung and plasma ceramide in COVID-19 linked to microvascular injury.JCI insight · 2023Article
- Differentiation in TCM patterns of chronic obstructive pulmonary disease by comprehensive metabolomic and lipidomic characterization.Frontiers in immunology · 2023Article
- Pharmacological sphingosine-1 phosphate receptor 1 targeting in cigarette smoke-induced emphysema in mice.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Endothelial cells in the pathogenesis of pulmonary arterial hypertension.The European respiratory journal · 2021Review
- Article
- Cigarette smoke extract affects methylation status and attenuates Sca-1 expression of mouse endothelial progenitor cell in vitro.Tobacco induced diseases · 2021Article
- Identification of lipid biomarker from serum in patients with chronic obstructive pulmonary disease.Respiratory research · 2020Article
- Smoking is associated with an improved short-term outcome in patients with rib fractures.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2020Article
- MicroRNA-126-3p Inhibits Angiogenic Function of Human Lung Microvascular Endothelial Cells via LAT1 (L-Type Amino Acid Transporter 1)-Mediated mTOR (Mammalian Target of Rapamycin) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Sphingolipids in COPD.European respiratory review : an official journal of the European Respiratory Society · 2019Review
- JAK2/STAT1-mediated HMGB1 translocation increases inflammation and cell death in a ventilator-induced lung injury model.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Role of Glucosylceramide in Lung Endothelial Cell Fate and Emphysema.American journal of respiratory and critical care medicine · 2019Article
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Prolonged exposure to cigarette smoking is the main risk factor for emphysema, a component of chronic obstructive pulmonary diseases (COPDs) characterized by destruction of alveolar walls. Moreover, smoking is associated with pulmonary artery remodeling and pulmonary hypertension, even in the absence of COPD, through as yet unexplained mechanisms. In murine models, elevations of intra- and paracellular ceramides in response to smoking have been implicated in the induction of lung endothelial cell apoptosis, but the role of ceramides in human cell counterparts is yet unknown. We modeled paracrine increases (outside-in) of palmitoyl ceramide (Cer16) in primary human lung microvascular cells. In naive cells, isolated from nonsmokers, Cer16 significantly reduced cellular proliferation and induced caspase-independent apoptosis via mitochondrial membrane depolarization, apoptosis-inducing factor translocation, and poly(ADP-ribose) polymerase cleavage. In these cells, caspase-3 was inhibited by ceramide-induced Akt phosphorylation, and by the induction of autophagic microtubule-associated protein-1 light-chain 3 lipidation. In contrast, cells isolated from smokers exhibited increased baseline proliferative features associated with lack of p16(INK4a) expression and Akt hyperphosphorylation. These cells were resistant to Cer16-induced apoptosis, despite presence of both endoplasmic reticulum stress response and mitochondrial membrane depolarization. In cells from smokers, the prominent up-regulation of Akt pathways inhibited ceramide-triggered apoptosis, and was associated with elevated sphingosine and high-mobility group box 1, skewing the cell's response toward autophagy and survival. In conclusion, the cell responses to ceramide are modulated by an intricate cross-talk between Akt signaling and sphingolipid metabolites, and profoundly modified by previous cigarette smoke exposure, which selects for an apoptosis-resistant phenotype.
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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.