ArticleMolecular biology reports2012
Beraprost sodium attenuates cigarette smoke extract-induced apoptosis in vascular endothelial cells.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- LRG1 promotes the apoptosis of pulmonary microvascular endothelial cells through KLK10 in chronic obstructive pulmonary disease.Tobacco induced diseases · 2024Article
- Significant role of circRNA BBS9 in chronic obstructive pulmonary disease via miRNA-103a-3p/BCL2L13.BMC pulmonary medicine · 2023Article
- Increased Thromboxane AMedicina (Kaunas, Lithuania) · 2023Article
- Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.Frontiers in medicine · 2023Review
- MiR-216a reduces apoptosis of pulmonary microvascular endothelial cells in COPD by targeting DNMT1.Tobacco induced diseases · 2023Article
- Long noncoding RNA HOTAIR facilitates pulmonary vascular endothelial cell apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD.Respiratory research · 2022Article
- Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation.Respiratory research · 2022Article
- Circ_0040929 Serves as Promising Biomarker and Potential Target for Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2022Article
- lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR-9a-5p/BCL2L11 axis in chronic obstructive pulmonary disease.Experimental and therapeutic medicine · 2021Article
- LncRNA MIR155HG contributes to smoke-related chronic obstructive pulmonary disease by targeting miR-128-5p/BRD4 axis.Bioscience reports · 2020Article
- Intercellular Communication by Vascular Endothelial Cell-Derived Extracellular Vesicles and Their MicroRNAs in Respiratory Diseases.Frontiers in molecular biosciences · 2020Review
- LINC00612/miR-31-5p/Notch1 Axis Regulates Apoptosis, Inflammation, and Oxidative Stress in Human Pulmonary Microvascular Endothelial Cells Induced by Cigarette Smoke Extract.International journal of chronic obstructive pulmonary disease · 2020Article
- Microarray Analysis of Long Non-Coding RNAs in Lung Tissues of Patients with COPD and HOXA-AS2 Promotes HPMECs Proliferation via Notch1.International journal of chronic obstructive pulmonary disease · 2020Article
- The Potential Roles of Exosomes in Chronic Obstructive Pulmonary Disease.Frontiers in medicine · 2020Review
- Cigarette Smoke Reduces Fatty Acid Catabolism, Leading to Apoptosis in Lung Endothelial Cells: Implication for Pathogenesis of COPD.Frontiers in pharmacology · 2019Article
- Notch1 regulates endothelial apoptosis via the ERK pathway in chronic obstructive pulmonary disease.American journal of physiology. Cell physiology · 2018Article
- miR-34a is involved in CSE-induced apoptosis of human pulmonary microvascular endothelial cells by targeting Notch-1 receptor protein.Respiratory research · 2018Article
- The role of the endothelium in asthma and chronic obstructive pulmonary disease (COPD).Respiratory research · 2017Review
- Notch signaling in lung diseases: focus on Notch1 and Notch3.Therapeutic advances in respiratory disease · 2016Review
- Dual effects of cigarette smoke extract on proliferation of endothelial progenitor cells and the protective effect of 5-aza-2'-deoxycytidine on EPCs against the damage caused by CSE.BioMed research international · 2014Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis is now widely recognized as an important part of chronic obstructive pulmonary disease (COPD) pathogenesis. Our previous study demonstrated that a prostacyclin (PGI(2)) analogue (beraprost sodium, BPS) prevented cigarette smoke extract (CSE) induced apoptosis of the pulmonary endothelium in rats. So we determined to clarify the apoptosis of vascular endothelial cells in COPD patient and the role of prostacyclin in the protection against apoptosis in vascular endothelial cells induced by CSE. Surgical specimens were obtained from 12 patients with COPD and 10 controls, and the level of apoptosis, prostacyclin synthase (PGI(2)S) expression and 6-keto-PGF1α (a stable metabolite of PGI(2)) were detected. The apoptotic index (AI), caspase-3 activity, expression of caspase-3 and 6-keto-PGF1α were examined in human umbilical vein endothelial cells (HUVECs) under exposure to varied concentrations of CSE for 24 h as well as under exposure to 2.5 % CSE for varied durations. Then, HUVECs under 2.5 % CSE were exposed to varied concentrations of BPS for 24 h and observed the alteration and the level of cAMP. Increased AI, decreased expression of PGI(2)S and 6-keto-PGF1α, were found in the lungs of patients with COPD compared with controls. Moreover, CSE induced apoptosis in means of both dose-dependent and time-dependent manners, and reduced the level of 6-keto-PGF1α in HUVECs. And with the treatment of BPS, an enhanced level of cAMP and decreased apoptosis were detected. The deficiency of PGI(2) critically contributes to the COPD-associated endothelial dysfunction and apoptosis. And BPS protects against the apoptosis in the vascular endothelial cells induced by CSE.
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