ArticleAmerican journal of translational research2017
COX-2 mediates PM2.5-induced apoptosis and inflammation in vascular endothelial cells.
Article in American journal of translational research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Airborne Particulate Matter as an Emerging Driver of Gastric Carcinogenesis: Molecular Pathways Linking Inflammation and Cancer.International journal of molecular sciences · 2026Review
- Persistent prostaglandin E2 upregulation and hormonal multi-resistance: A hypothesis for long COVID.Biochemistry and biophysics reports · 2026Article
- Health Risk and Pathogenesis of PMToxics · 2026Review
- The silent threat: effects of PM2.5 exposure on perinatal complications and neonatal outcomes.BMC pregnancy and childbirth · 2025Article
- ATF3 mediates PM2.5-induced apoptosis and inflammation in ovarian granulosa cells.Journal of ovarian research · 2024Article
- Vascular endothelial dysfunction induced by 3-bromofluoranthene via MAPK-mediated-NFκB pro-inflammatory pathway and intracellular ROS generation.Archives of toxicology · 2024Article
- Article
- Glucocorticoids alleviate particulate matter-induced COX-2 expression and mitochondrial dysfunction through the Bcl-2/GR complex in A549 cells.Scientific reports · 2023Article
- Article
- Genetic factors involved in the co‑occurrence of endometriosis with ankylosing spondylitis (Review).Molecular medicine reports · 2023Review
- Cell Death Pathways: The Variable Mechanisms Underlying Fine Particulate Matter-Induced Cytotoxicity.ACS nanoscience Au · 2023Review
- Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.Frontiers in medicine · 2023Review
- Development of pharmacotherapies for abdominal aortic aneurysms.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Ketorolac tromethamine alleviates IL-1β-induced chondrocyte injury by inhibiting COX-2 expression.Experimental and therapeutic medicine · 2022Article
- Inhibitory effect of main phenolic acid components ofFrontiers in pharmacology · 2022Article
- Global research trends in atherosclerosis: A bibliometric and visualized study.Frontiers in cardiovascular medicine · 2022Article
- Mechanisms of cardiovascular toxicity induced by PMEnvironmental science and pollution research international · 2021Review
- Schisandrae Fructus ethanol extract attenuates particulate matter 2.5-induced inflammatory and oxidative responses by blocking the activation of the ROS-dependent NF-κB signaling pathway.Nutrition research and practice · 2021Article
- Celecoxib alleviates pathological cardiac hypertrophy and fibrosis via M1-like macrophage infiltration in neonatal mice.iScience · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence demonstrated that particulate matter 2.5 (PM2.5) exposure served as an important risk factor of cardiovascular diseases. Some studies also reported that COX-2/mPGES-1/PGE2 cascade played a pathogenic role in vascular injury. However, the relationship between the PM2.5 exposure and the activation of COX-2/mPGES-1/PGE2 cascade in endothelial cells is still unknown. In the present study, mouse aorta endothelial cells were exposed to PM2.5. Strikingly, following the PM2.5 treatment, we observed dose- and time-dependent upregulation of COX-2 at both protein and mRNA levels as determined by Western blotting and qRT-PCR, respectively. However, COX-1 mRNA expression was not affected by PM2.5 treatment. Next, we examined mPGES-1 expression. As expected, mPGES-1 protein was markedly increased by PM2.5 exposure in line with a significant increment of PGE2 release in medium. At the same time, we observed a dose-dependent upregulation of another two PGE2 synthases of mPGES-2 and cPGES determined by qRT-PCR. Inhibition of COX-2 by using a specific COX-2 inhibitor NS-398 markedly blocked cell apoptosis, inflammation, and PGE2 secretion. Taken together, these results suggested that PM2.5 could activate inflammatory axis of COX-2/PGES/PGE2 in vascular endothelial cells to promote cell apoptosis and inflammatory response.
Indexed as
Identifiers
28979673PMC5622242W2981143265What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.