ArticleTobacco induced diseases2020
Inhibiting DNA methylation alleviates cigarette smoke extract-induced dysregulation of Bcl-2 and endothelial apoptosis.
Article in Tobacco induced diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- <p>Cigarette smoke combined withMolecular medicine reports · 2026Article
- Cellular and Molecular Mechanisms of Vascular Endothelial Injury Induced by Cigarette Smoke and Cigarette Smoke Extract in Atherosclerosis.Journal of inflammation research · 2026Review
- The role of Bcl‑2 in controlling the transition between autophagy and apoptosis (Review).Molecular medicine reports · 2025Review
- The Impact of Modifiable Risk Factors on the Endothelial Cell Methylome and Cardiovascular Disease Development.Frontiers in bioscience (Landmark edition) · 2025Review
- Therapeutic effects of melatonin on the lungs of rats exposed to passive smoking.Respiratory research · 2024Article
- Long noncoding RNA HOTAIR facilitates pulmonary vascular endothelial cell apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD.Respiratory research · 2022Article
- The role of cigarette smoke-induced pulmonary vascular endothelial cell apoptosis in COPD.Respiratory research · 2021Review
- The Ganglioside Monosialotetrahexosylganglioside Protects Auditory Hair Cells Against Neomycin-Induced Cytotoxicity Through Mitochondrial Antioxidation: AnFrontiers in cellular neuroscience · 2021Article
- Reactivation of oncogenes involved in G1/S transcription and apoptosis pathways by low dose decitabine promotes HT29 human colon cancer cell growth in vitro.American journal of translational research · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThere is evidence that cigarette smoking participates in disease progression through endothelial apoptosis. Bcl-2 family proteins are essential and critical regulators of apoptosis. We explored whether Bcl-2 plays a role in cigarette smoke extract induced (CSE-induced) endothelial apoptosis. Furthermore, given the involvement of epigenetics in apoptosis and Bcl-2 expression, we hypothesized that CSE-induced apoptosis might be caused by gene methylation.
methodsHuman umbilical vascular endothelial cells (HUVECs) were treated with CSE, CSE plus 5-aza-2'-deoxycytidine (AZA, an inhibitor of DNA methylation), or AZA and phosphate-buffered saline (PBS). Endothelial apoptosis was determined by Annexin-V and propidium iodide staining. The expression levels of Bcl-2, Bax, and cytochrome C (cyt C) were assessed by immunoblotting and RT-PCR. The methylation status of the Bcl-2 promoter was observed by bisulfite sequencing PCR (BSP).
resultsThe apoptotic index of endothelial cells in the CSE-treated group increased. Decreased expression of Bcl-2 and high methylation of the Bcl-2 promoter were observed after CSE treatment. AZA alleviated the endothelial apoptosis caused by CSE. AZA treatment also increased Bcl-2 expression along with decreased Bcl-2 promoter methylation.
conclusionsInhibiting DNA methylation alleviates CSE-induced endothelial apoptosis and Bcl-2 promoter methylation. Bcl-2 promoter methylation might be involved in CES-induced endothelial apoptosis.
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