ArticleAmerican journal of respiratory cell and molecular biology2011
Neutral sphingomyelinase 2: a novel target in cigarette smoke-induced apoptosis and lung injury.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 82 citations in OpenAlex.
- Lipid Metabolism and Obesity in Early Life: Drivers of Chronic Lung Disease From Development to Adulthood.Molecular nutrition & food research · 2026Review
- Extracellular vesicular delivery of ceramides from pulmonary macrophages to endothelial cells facilitates chronic obstructive pulmonary disease.Cell communication and signaling : CCS · 2025Article
- Beyond type 2 asthma biomarkers: risk stratification for NSAID-exacerbated respiratory disease.ERJ open research · 2024Article
- New Therapeutic Options in Pulmonal Diseases: Sphingolipids and Modulation of Sphingolipid Metabolism.Handbook of experimental pharmacology · 2024Review
- Plasma sphingolipids, lung function and COPD: the Cardiovascular Health Study.ERJ open research · 2023Article
- Lipid-lowering drugs affect lung cancer risk via sphingolipid metabolism: a drug-target Mendelian randomization study.Frontiers in genetics · 2023Article
- Cigarette Smoke Extract Induces p38 MAPK-Initiated, Fas-Mediated Eryptosis.International journal of molecular sciences · 2022Article
- Pharmacological sphingosine-1 phosphate receptor 1 targeting in cigarette smoke-induced emphysema in mice.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Epithelial IL-33 appropriates exosome trafficking for secretion in chronic airway disease.JCI insight · 2021Article
- Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy.Respiratory research · 2021Article
- Ceramide induces MMP-9 expression through JAK2/STAT3 pathway in airway epithelium.Lipids in health and disease · 2020Article
- Distinctive lipid signatures of bronchial epithelial cells associated with cystic fibrosis drugs, including Trikafta.JCI insight · 2020Article
- Airway Resistance Caused by Sphingomyelin Synthase 2 Insufficiency in Response to Cigarette Smoke.American journal of respiratory cell and molecular biology · 2020Article
- Iron and Sphingolipids as Common Players of (Mal)Adaptation to Hypoxia in Pulmonary Diseases.International journal of molecular sciences · 2020Review
- Sphingolipids in COPD.European respiratory review : an official journal of the European Respiratory Society · 2019Review
- Transcriptomics of atopy and atopic asthma in white blood cells from children and adolescents.The European respiratory journal · 2019Article
- Ceramide and Regulation of Vascular Tone.International journal of molecular sciences · 2019Review
- Neutrophil elastase correlates with increased sphingolipid content in cystic fibrosis sputum.Pediatric pulmonology · 2018Article
- The role of sphingolipids in psychoactive drug use and addiction.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Surfactant Protein D Deficiency Aggravates Cigarette Smoke-Induced Lung Inflammation by Upregulation of Ceramide Synthesis.Frontiers in immunology · 2018Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is caused by exposure to cigarette smoke (CS). One mechanism of CS-induced lung injury is aberrant generation of ceramide, which leads to elevated apoptosis of epithelial and endothelial cells in the alveolar spaces. Recently, we discovered that CS-induced ceramide generation and apoptosis in pulmonary cells is governed by neutral sphingomyelinase (nSMase) 2. In the current experiments, we expanded our studies to investigate whether nSMase2 governs ceramide generation and apoptosis in vivo using rodent and human models of CS-induced lung injury. We found that exposure of mice or rats to CS leads to colocalizing elevations of ceramide levels and terminal deoxynucleotidyl transferase mediated X-dUTP nick end labeling-positive cells in lung tissues. These increases are nSMase2 dependent, and are abrogated by treatment with N-acetyl cysteine or anti-nSMase2 small interfering RNA (siRNA). We further showed that mice that are heterozygous for nSMase2 demonstrate significant decrease in ceramide generation after CS exposure, whereas acidic sphingomyelinase (aSMase) knockout mice maintain wild-type ceramide levels, confirming our previous findings (in human airway epithelial cells) that only nSMase2, and not aSMase, is activated by CS exposure. Lastly, we found that lung tissues from patients with emphysema (smokers) display significantly higher levels of nSMase2 expression compared with lung tissues from healthy control subjects. Taken together, these data establish the central in vivo role of nSMase2 in ceramide generation, aberrant apoptosis, and lung injury under CS exposure, underscoring its promise as a novel target for the prevention of CS-induced airspace destruction.
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