ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
p53- and PAI-1-mediated induction of C-X-C chemokines and CXCR2: importance in pulmonary inflammation due to cigarette smoke exposure.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- PAI-1 Inhibitor TM5441 Attenuates Emphysema and Airway Inflammation in a Murine Model of Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2025Article
- Genomic Locus Tagged by Lung Function GWAS SNV rs12477314 (2q37.3) Acts as a Regulatory Region for a Systemic Inflammatory Phenotype.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Chronic Exposure to Two Regimens of Waterpipe Smoke Elicits Lung Injury, Genotoxicity, and Mitochondrial Impairment with the Involvement of MAPKs Activation in Mice.International journal of molecular sciences · 2025Article
- p53: A player in the tumor microenvironment.Oncology research · 2025Review
- Mechanism underlying the therapeutic effects of effective component compatibility of Bufei Yishen formula III combined with exercise rehabilitation on chronic obstructive pulmonary disease.Annals of medicine · 2024Article
- Analysis of network expression and immune infiltration of disulfidptosis-related genes in chronic obstructive pulmonary disease.Immunity, inflammation and disease · 2024Article
- Identification of novel biomarkers related to neutrophilic inflammation in COPD.Frontiers in immunology · 2024Article
- CSE reduces OTUD4 triggering lung epithelial cell apoptosis via PAI-1 degradation.Cell death & disease · 2023Article
- Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury: the Small Player with Big Actions.Molecular neurobiology · 2023Review
- Secreted Cytokines within the Urine of AKI Patients Modulate TP53 and SIRT1 Levels in a Human Podocyte Cell Model.International journal of molecular sciences · 2023Article
- Knockdown of GNL3L Alleviates the Progression of COPD Through Inhibiting the ATM/p53 Pathway.International journal of chronic obstructive pulmonary disease · 2023Article
- The Potential Importance of CXCL1 in the Physiological State and in Noncancer Diseases of the Cardiovascular System, Respiratory System and Skin.International journal of molecular sciences · 2022Review
- Article
- Combining p53 mRNA nanotherapy with immune checkpoint blockade reprograms the immune microenvironment for effective cancer therapy.Nature communications · 2022Article
- Pulmonary toxicity and gene expression changes in response to whole-body inhalation exposure to multi-walled carbon nanotubes in rats.Inhalation toxicology · 2022Article
- Emerging Biological Functions of IL-17A: A New Target in Chronic Obstructive Pulmonary Disease?Frontiers in pharmacology · 2021Review
- The P72R Polymorphism in R248Q/W p53 Mutants Modifies the Mutant Effect on Epithelial to Mesenchymal Transition Phenotype and Cell Invasion via CXCL1 Expression.International journal of molecular sciences · 2020Article
- miR-223: A Key Regulator in the Innate Immune Response in Asthma and COPD.Frontiers in medicine · 2020Review
- Monocyte Response to DifferentToxins · 2018Article
- Regulation of p53-mediated changes in the uPA-fibrinolytic system and in lung injury by loss of surfactant protein C expression in alveolar epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
We previously demonstrated that tumor suppressor protein p53 augments plasminogen activator inhibitor-1 (PAI-1) expression in alveolar epithelial cells (AECs) during chronic cigarette smoke (CS) exposure-induced lung injury. Chronic lung inflammation with elevated p53 and PAI-1 expression in AECs and increased susceptibility to and exacerbation of respiratory infections are all associated with chronic obstructive pulmonary disease (COPD). We recently demonstrated that preventing p53 from binding to the endogenous PAI-1 mRNA in AECs by either suppressing p53 expression or blockading p53 interactions with the PAI-1 mRNA mitigates apoptosis and lung injury. Within this context, we now show increased expression of the C-X-C chemokines (CXCL1 and CXCL2) and their receptor CXCR2, and the intercellular cellular adhesion molecule-1 (ICAM-1), in the lung tissues of patients with COPD. We also found a similar increase in lung tissues and AECs from wild-type (WT) mice exposed to passive CS for 20 wk and in primary AECs treated with CS extract in vitro. Interestingly, passive CS exposure of mice lacking either p53 or PAI-1 expression resisted an increase in CXCL1, CXCL2, CXCR2, and ICAM-1. Furthermore, inhibition of p53-mediated induction of PAI-1 expression by treatment of WT mice exposed to passive CS with caveolin-1 scaffolding domain peptide reduced CXCL1, CXCL2, and CXCR2 levels and lung inflammation. Our study reveals that p53-mediated induction of PAI-1 expression due to chronic CS exposure exacerbates lung inflammation through elaboration of CXCL1, CXCL2, and CXCR2. We further provide evidence that targeting this pathway mitigates lung injury associated with chronic CS exposure.
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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.