ArticleScientific reports2021
Gender specific airway gene expression in COPD sub-phenotypes supports a role of mitochondria and of different types of leukocytes.
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 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Integrative multi-omics identifies CYP1B1 as a candidate molecular link between toxicant exposure and ferroptosis-related epithelial stress in COPD.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Mitochondrial reprogramming of neutrophil extracellular traps in chronic obstructive pulmonary disease and asthma: toward a phenotype-driven therapeutic framework.Frontiers in immunology · 2026Review
- Identification and validation of palmitoylation-related biomarkers in gestational diabetes mellitus.Scientific reports · 2025Article
- Gut Microbiome and Transcriptomic Changes in Cigarette Smoke-Exposed Mice Compared to COPD and CD Patient Datasets.International journal of molecular sciences · 2024Article
- MNDA, a PYHIN factor involved in transcriptional regulation and apoptosis control in leukocytes.Frontiers in immunology · 2024Review
- Mitochondrial Dynamics in Pulmonary Hypertension.Biomedicines · 2023Review
- Mitochondria in health, disease, and aging.Physiological reviews · 2023Review
- Recent evidence from omic analysis for redox signalling and mitochondrial oxidative stress in COPD.Journal of inflammation (London, England) · 2022Review
- Article
- Proteomic profiling of serum identifies a molecular signature that correlates with clinical outcomes in COPD.PloS one · 2022Article
- Dynamically upregulated mast cell CPA3 patterns in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis.Frontiers in immunology · 2022Article
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Authors and funding
48 authors at 19 institutions in 8 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic obstructive pulmonary disease (COPD) is a destructive inflammatory disease and the genes expressed within the lung are crucial to its pathophysiology. We have determined the RNAseq transcriptome of bronchial brush cells from 312 stringently defined ex-smoker patients. Compared to healthy controls there were for males 40 differentially expressed genes (DEGs) and 73 DEGs for females with only 26 genes shared. The gene ontology (GO) term "response to bacterium" was shared, with several different DEGs contributing in males and females. Strongly upregulated genes TCN1 and CYP1B1 were unique to males and females, respectively. For male emphysema (E)-dominant and airway disease (A)-dominant COPD (defined by computed tomography) the term "response to stress" was found for both sub-phenotypes, but this included distinct up-regulated genes for the E-sub-phenotype (neutrophil-related CSF3R, CXCL1, MNDA) and for the A-sub-phenotype (macrophage-related KLF4, F3, CD36). In E-dominant disease, a cluster of mitochondria-encoded (MT) genes forms a signature, able to identify patients with emphysema features in a confirmation cohort. The MT-CO2 gene is upregulated transcriptionally in bronchial epithelial cells with the copy number essentially unchanged. Both MT-CO2 and the neutrophil chemoattractant CXCL1 are induced by reactive oxygen in bronchial epithelial cells. Of the female DEGs unique for E- and A-dominant COPD, 88% were detected in females only. In E-dominant disease we found a pronounced expression of mast cell-associated DEGs TPSB2, TPSAB1 and CPA3. The differential genes discovered in this study point towards involvement of different types of leukocytes in the E- and A-dominant COPD sub-phenotypes in males and females.
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