ArticleScientific reports2019
LKB1/p53/TIGAR/autophagy-dependent VEGF expression contributes to PM2.5-induced pulmonary inflammatory responses.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 34 citations in OpenAlex.
- Molecular insights and therapeutic implications for the tumor suppressor role of LKB1 in non-small cell lung cancer.Cancer letters · 2026Review
- Micro-Nanoplastic Exposure and Lung Cancer Biomarkers: The Role of Extracellular Vesicle-Mediated Intercellular Communication.International journal of molecular sciences · 2026Review
- The Impact of Environmental Pollution and Climate Change on Allergic Rhinitis and Lung Diseases.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- A novel piperine derivative HJ-23 exhibits anti-colorectal cancer effects by activating the p53 pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The role of PM2.5 exposure in lung cancer: mechanisms, genetic factors, and clinical implications.EMBO molecular medicine · 2025Review
- Disruption of TIGAR-TAK1 alleviates immunopathology in a murine model of sepsis.Nature communications · 2024Article
- Induction of heme oxygenase-1 antagonizes PM2.5-induced pulmonary VEGFA expression through regulating HIF-1α.Journal of biochemical and molecular toxicology · 2023Article
- Identification of differentially expressed genes and pathways in BEAS-2B cells upon long-term exposure to particulate matter (PMEnvironmental health and preventive medicine · 2023Article
- Adverse effects of air pollution-derived fine particulate matter on cardiovascular homeostasis and disease.Trends in cardiovascular medicine · 2022Review
- TIGAR alleviates oxidative stress in brain with extended ischemia via a pentose phosphate pathway-independent manner.Redox biology · 2022Article
- Insights from the p53 induced TIGAR protein 2 in the glycolytic pathway model.Bioinformation · 2022Article
- The role of TIGAR in nervous system diseases.Frontiers in aging neuroscience · 2022Review
- REDD1 (regulated in development and DNA damage-1)/autophagy inhibition ameliorates fine particulate matter (PM2.5) -induced inflammation and apoptosis in BEAS-2B cells.Bioengineered · 2021Article
- Structure, regulation, and biological functions of TIGAR and its role in diseases.Acta pharmacologica Sinica · 2021Review
- Ovarian hormones-autophagy-immunity axis in menstruation and endometriosis.Theranostics · 2021Review
- Astragaloside IV Protects from PM2.5-Induced Lung Injury by Regulating Autophagy via Inhibition of PI3K/Akt/mTOR Signaling in vivo and in vitro.Journal of inflammation research · 2021Article
- lncRNA Gm16410 Mediates PMFrontiers in cell and developmental biology · 2021Article
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the health hazards of PM2.5 exposure is to induce pulmonary inflammatory responses. In our previous study, we demonstrated that exposing both the immortalized and primary human bronchial epithelial cells to PM2.5 results in a significant upregulation of VEGF production, a typical signaling event to trigger chronic airway inflammation. Further investigations showed that PM2.5 exposure strongly induces ATR/CHK1/p53 cascade activation, leading to the induction of DRAM1-dependent autophagy to mediate VEGF expression by activating Src/STAT3 pathway. In the current study, we further revealed that TIGAR was another transcriptional target of p53 to trigger autophagy and VEGF upregulation in Beas-2B cells after PM2.5 exposure. Furthermore, LKB1, but not ATR and CHK1, played a critical role in mediating p53/TIGAR/autophagy/VEGF pathway activation also by linking to Src/STAT3 signaling cascade. Therefore, on combination of the previous report, we have identified both ATR/CHK1/p53/DRAM1- and LKB1/p53/TIGAR- dependent autophagy in mediating VEGF production in the bronchial epithelial cells under PM2.5 exposure. Moreover, the in vivo study further confirmed VEGF induction in the airway potentially contributed to the inflammatory responses in the pulmonary vascular endothelium of PM2.5-treated rats. Therefore, blocking VEGF expression or autophagy induction might be the valuable strategies to alleviating PM2.5-induced respiratory injuries.
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