ArticleJournal of thoracic disease2017
The role of cyclooxygenase-2 in the protection against apoptosis in vascular endothelial cells induced by cigarette smoking.
Article in Journal of thoracic disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Modelling cigarette smoke-induced lung vascular dysfunction using an alveolus-on-chip.Materials today. Bio · 2026Article
- Oscillatory Disturbed Flow Enhances Inflammatory and Oxidative Stress Markers in Endothelial Cells.Methods and protocols · 2025Article
- Succinate Regulates Endothelial Mitochondrial Function and Barrier Integrity.Antioxidants (Basel, Switzerland) · 2024Article
- The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis.International journal of molecular sciences · 2023Review
- EPC-exosomal miR-26a-5p improves airway remodeling in COPD by inhibiting ferroptosis of bronchial epithelial cells via PTGS2/PGE2 signaling pathway.Scientific reports · 2023Article
- Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.Frontiers in medicine · 2023Review
- Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation.Respiratory research · 2022Article
- Increased Serum Levels of Matrix-metalloproteinase-9, Cyclo-oxygenase-2 and Prostaglandin E-2 in Patients with Chronic Obstructive Pulmonary Disease (COPD).Indian journal of clinical biochemistry : IJCB · 2022Article
- Prohibitin Protects Pulmonary Microvascular Endothelial Cells Against Cigarette Smoke Extract-Induced Cell Apoptosis and Inflammation.International journal of chronic obstructive pulmonary disease · 2022Article
- Low-dose aspirin and incidence of lung carcinoma in patients with chronic obstructive pulmonary disease in Hong Kong: A cohort study.PLoS medicine · 2022Article
- Inhibition of cyclooxygenase-2 enhanced intestinal epithelial homeostasis via suppressing β-catenin signalling pathway in experimental liver fibrosis.Journal of cellular and molecular medicine · 2021Article
- The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD.Respiratory research · 2021Review
- Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy.Respiratory research · 2021Article
- Influence of Active Exposure to Tobacco Smoke on Nitric Oxide Status of Pregnant Women.International journal of environmental research and public health · 2018Article
- Differential exposure and acute health impacts of inhaled solid-fuel emissions from rudimentary and advanced cookstoves in female CD-1 mice.Environmental research · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundApoptosis has been demonstrated to be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD). Cyclooxygenase-2 (COX-2) seems to be biologically relevant in COPD. However, the role of COX-2 in the apoptosis in vascular endothelial cells induced by cigarette smoke extract (CSE) remains to be elucidated. Our recent study found that the prostacyclin, one of the COX products in the microvascular endothelium, inhibited apoptosis in the emphysematous lungs of rats induced by CSE. In order to clarify the role of COX-2 in the apoptosis of vascular endothelial cells induced by CSE, we performed the present experiment to elucidate it.
methodsTwenty surgical lung specimens were obtained from 6 patients with COPD, 7 smoking controls and seven nonsmoking controls. The apoptotic index (AI) and COX-2 protein expression were detected in lung tissues. To further investigate the effects of CSE on the apoptosis and COX-2 expression in a human vascular endothelial cell line, the apoptosis rate and COX-2 expression were examined in human umbilical vein endothelial cells (ECV304) under exposure to varied concentrations of CSE as well as under exposure to 5.0% CSE for varied durations. Repeatedly, the apoptosis rate and COX-2 expression in ECV304 cells under 5.0% CSE were examined after exposing to varied concentrations of celecoxib, a highly selective COX-2 inhibitor.
resultsSignificantly increased AI and expression of COX-2 were found both in the lungs of patients with COPD and smoking controls compared with nonsmoking controls. The CSE induced apoptosis in ECV304 cells in means of both dose-dependent and time-dependent manners. The COX-2 was slightly expressed in the cells after exposing to 5% CSE for 3 and 6 h, and markedly expressed after the exposure time for 9 and 12 h, but vanished after 24 h of the exposure. Of interest, with the completely block of the COX-2 expression by celecoxib at 50.0 µmol/L, the apoptosis rate was markedly increased again in ECV304 cells under exposure to 5.0% CSE.
conclusionsEndothelial cell apoptosis and the expression of COX-2 protein were increased in both COPD patients and CSE-induced vascular endothelial cells. Of interest, it seems that the COX-2 probably had a protective role against the apoptosis in the vascular endothelial cells induced by cigarette smoking.
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