ArticleAmerican journal of physiology. Cell physiology2018
Notch1 regulates endothelial apoptosis via the ERK pathway in chronic obstructive pulmonary disease.
Article in American journal of physiology. Cell physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 72 citations in OpenAlex.
- Ticagrelor IncreasesInternational journal of molecular sciences · 2020Trial
- Article
- Wenshen Yiqi Granule Alleviates Chronic Obstructive Pulmonary Disease via the Long Noncoding RNA-XIST/MicroRNA-200c-3p Axis.Pulmonary circulation · 2025Article
- Acute exposure to electronic cigarette components alters mRNA expression of pre-osteoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- MAPK4 facilitates angiogenesis by inhibiting the ERK pathway in non-small cell lung cancer.Cancer innovation · 2024Article
- Upregulation of Notch Signaling and Cell-Differentiation Inhibitory Transcription Factors in Stable Chronic Obstructive Pulmonary Disease Patients.International journal of molecular sciences · 2024Article
- Mitochondrial damage-associated molecular patterns in chronic obstructive pulmonary disease: Pathogenetic mechanism and therapeutic target.Journal of translational internal medicine · 2023Article
- Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers.Antioxidants (Basel, Switzerland) · 2023Review
- Long noncoding RNA HOTAIR facilitates pulmonary vascular endothelial cell apoptosis via DNMT1 mediated hypermethylation of Bcl-2 promoter in COPD.Respiratory research · 2022Article
- Notch1 activation of Jagged1 contributes to differentiation of mesenchymal stem cells into endothelial cells under cigarette smoke extract exposure.BMC pulmonary medicine · 2022Article
- Seven ferroptosis-specific expressed genes are considered as potential biomarkers for the diagnosis and treatment of cigarette smoke-induced chronic obstructive pulmonary disease.Annals of translational medicine · 2022Article
- PECAM EMPs regulate apoptosis in pulmonary microvascular endothelial cells in COPD by activating the Akt signaling pathway.Tobacco induced diseases · 2022Article
- The Notch pathway attenuates burn-induced acute lung injury in rats by repressing reactive oxygen species.Burns & trauma · 2022Article
- Autophagy Induced by BCL2-Related ceRNA Network Participates in the Occurrence of COPD.International journal of chronic obstructive pulmonary disease · 2022Article
- Prohibitin Protects Pulmonary Microvascular Endothelial Cells Against Cigarette Smoke Extract-Induced Cell Apoptosis and Inflammation.International journal of chronic obstructive pulmonary disease · 2022Article
- ERK: A Double-Edged Sword in Cancer. ERK-Dependent Apoptosis as a Potential Therapeutic Strategy for Cancer.Cells · 2021Review
- Notch3: A New Culprit in Fibrotic Lung Disease.American journal of respiratory cell and molecular biology · 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
- Mitochondrial Fission Mediated Cigarette Smoke-induced Pulmonary Endothelial Injury.American journal of respiratory cell and molecular biology · 2020Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Notch signaling pathway plays critical role for determining cell fate by controlling proliferation, differentiation, and apoptosis. In the current study, we investigated the roles of the Notch signaling pathway in cigarette smoke (CS)-induced endothelial apoptosis in chronic obstructive pulmonary disease (COPD). We obtained surgical specimens from 10 patients with COPD and 10 control participants. Notch1, 2, and 4 express in endothelial cells, whereas Notch3 mainly localizes in smooth muscle cells. Compared with control groups, we found that the expression of Notch1, 3, and 4 decreased, as well as their target genes Hes1 and Hes2, while the expression of Notch2 and extracellular signal-regulated kinase (ERK)1/2 increased in COPD patients compared with controls, as well as in human pulmonary microvascular endothelial cells (HPMECs) when exposed to CS extract (CSE). Overexpression of Notch1 with N1ICD in HPMECs markedly alleviated the cell apoptosis induced by CSE. The ERK signaling pathway was significantly activated by CSE, which correlated with CSE-induced apoptosis. However, this activation can be abolished by N1ICD overexpression. Furthermore, treatment of PD98059 (ERK inhibitor) significantly alleviated CSE-induced apoptosis, as well as reduced the methylation of mitochondrial transcription factor A (mtTFA) promoter, which was correlated with CS-induced endothelial apoptosis. These results suggest that CS alters Notch signaling in pulmonary endothelial cells. Notch1 protects against CS-induced endothelial apoptosis in COPD through inhibiting the ERK pathway, while the ERK pathway further regulates the methylation of mtTFA promotor.
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