ArticleRespiratory research2018
miR-34a is involved in CSE-induced apoptosis of human pulmonary microvascular endothelial cells by targeting Notch-1 receptor protein.
Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- The Role of MicroRNAs Implicated in the Regulation of PI3K/AKT and Focal Adhesion Signaling Pathways in Chronic Obstructive Pulmonary Disease.Biochemical genetics · 2026Article
- BMSCs exosomes regulate pulmonary microvascular endothelial apoptosis via circRNA_43350/miR-342-5p in COPD.Scientific reports · 2026Article
- Pathogenesis and clinical management of chronic multilobar segmental bronchial stenosis: a literature review.European journal of medical research · 2025Review
- POFUT1 as a cancer biomarker: insights into its oncogenic mechanisms and clinical relevance.Journal of molecular medicine (Berlin, Germany) · 2025Review
- MicroRNAs as promising drug delivery target to ameliorate chronic obstructive pulmonary disease using nano-carriers: a comprehensive review.Molecular and cellular biochemistry · 2025Review
- miRNA Signatures in Alveolar Macrophages Related to Cigarette Smoke: Assessment and Bioinformatics Analysis.International journal of molecular sciences · 2025Article
- Differential miRNA Profiling Reveals miR-4433a-5p as a Key Regulator of Chronic Obstructive Pulmonary Disease Progression via PIK3R2- mediated Phenotypic Modulation.Combinatorial chemistry & high throughput screening · 2024Article
- MiRNA-210 is involved in cigarette smoke extract-induced apoptosis of MLE-12 via the Shh signaling pathway.Tobacco induced diseases · 2024Article
- Investigating the link between miR-34a-5p and TLR6 signaling in sepsis-induced ARDS.3 Biotech · 2023Article
- MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1.Tobacco induced diseases · 2023Article
- CSE regulates LINC000665/XBP-1 in the progress of pulmonary fibrosis.Tobacco induced diseases · 2023Article
- Review
- The Polyvalent Role of NF90 in RNA Biology.International journal of molecular sciences · 2022Review
- Identification and validation of aging-related genes in COPD based on bioinformatics analysis.Aging · 2022Article
- Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?International journal of molecular sciences · 2022Review
- Prohibitin Protects Pulmonary Microvascular Endothelial Cells Against Cigarette Smoke Extract-Induced Cell Apoptosis and Inflammation.International journal of chronic obstructive pulmonary disease · 2022Article
- The Novel Regulatory Role of the lncRNA-miRNA-mRNA Axis in Chronic Inflammatory Airway Diseases.Frontiers in molecular biosciences · 2022Review
- Transcription Factor p300 Regulated miR-451b Weakens the Cigarette Smoke Extract-Induced Cellular Stress by Targeting RhoA/ROCK2 Signaling.Oxidative medicine and cellular longevity · 2022Article
- Pulmonary MicroRNA Changes Alter Angiogenesis in Chronic Obstructive Pulmonary Disease and Lung Cancer.Biomedicines · 2021Article
- The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD.Respiratory research · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAbnormal apoptosis of lung endothelial cells has been observed in emphysematous lung tissue and has been suggested to be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD). Studies have shown that microRNAs (miRNAs) contribute to the pathogenesis of pulmonary diseases by regulating cell apoptosis. The present study was designed to investigate the expression of microRNA-34a (miR-34a) in human pulmonary microvascular endothelial cells (HPMECs) exposed to cigarette smoke extract (CSE), and the potential regulatory role of miR-34a in endothelial cell apoptosis.
resultsOur results showed that the expression of miR-34a was significantly increased in CSE-treated HPMECs, and inhibiting miR-34a attenuated CSE-induced HPMEC apoptosis. Furthermore, expression of Notch-1, a receptor protein in the Notch signalling pathway, was decreased and was inversely correlated with miR-34a expression in HPMECs treated with CSE. Computational miRNA target prediction confirmed that Notch-1 is a target of miR-34a. Luciferase reporter assay further confirmed the direct interaction between miR-34a and the 3'-untranslated region (UTR) of Notch-1. Restoration of Notch-1 pathway was able to partially block the effect of miR-34a on HPMEC apoptosis. These results indicate that Notch-1 is a critical downstream target of miR-34a in regulating the CSE-induced HPMEC apoptosis.
conclusionsOur results suggest that miR-34a plays a key role in CSE-induced endothelial cell apoptosis by directly regulating its target gene Notch-1 in endothelial cells.
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