ArticleInternational journal of molecular sciences2015
Leptin Promotes cPLA₂ Gene Expression through Activation of the MAPK/NF-κB/p300 Cascade.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Acute Strenuous Exercise Induces an Imbalance on Histone H4 Acetylation/Histone Deacetylase 2 and Increases the Proinflammatory Profile of PBMC of Obese Individuals.Oxidative medicine and cellular longevity · 2017Trial
- P300 in Inflammation: An Updated Perspective on Its Molecular Mechanisms and Therapeutic Potential.Inflammation · 2026Review
- Leptin, Interleukin 6, and Vascular Endothelial Growth Factor as Potential Predictors of Primary Hypertension in Children and Adolescents with Obesity.International journal of molecular sciences · 2026Article
- Proarrhythmic Lipid Inflammatory Mediators: Mechanisms in Obesity Arrhythmias.Journal of cellular physiology · 2025Review
- The Potential of Metabolomics as a Tool for Identifying Biomarkers Associated with Obesity and Its Complications: A Scoping Review.International journal of molecular sciences · 2024Article
- Evaluation of Selected Pro- and Anti-Inflammatory Adipokines in Colostrum from Mothers with Gestational Diabetes Mellitus.International journal of molecular sciences · 2024Observational
- Respiratory issues in patients with multiple sclerosis as a risk factor during SARS-CoV-2 infection: a potential role for exercise.Molecular and cellular biochemistry · 2023Review
- Protective role of zinc in the pathogenesis of respiratory diseases.European journal of clinical nutrition · 2023Review
- The Role of Adipokines in Inflammatory Mechanisms of Obesity.International journal of molecular sciences · 2022Review
- TNF-Oxidative medicine and cellular longevity · 2022Article
- TGF-β: The missing link in obesity-associated airway diseases?Current research in pharmacology and drug discovery · 2021Review
- Adipokines and Obesity. Potential Link to Metabolic Disorders and Chronic Complications.International journal of molecular sciences · 2020Review
- PCNA and JNK1-Stat3 pathways respectively promotes and inhibits diabetes-associated centrosome amplification by targeting at the ROCK1/14-3-3σ complex in human colon cancer HCT116 cells.Journal of cellular physiology · 2019Article
- Participation of NADPH Oxidase-Related Reactive Oxygen Species in Leptin-Promoted Pulmonary Inflammation: Regulation of cPLA2α and COX-2 Expression.International journal of molecular sciences · 2019Article
- Lipopolysaccharide promoted proliferation and adipogenesis of preadipocytes through JAK/STAT and AMPK-regulated cPLA2 expression.International journal of medical sciences · 2019Article
- [Relationship between cytoplasmic phospholipase A2 and nuclear factor κB in one lung ventilation-induced lung injury in rabbits].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperplasia or hypertrophy of adipose tissues plays a crucial role in obesity, which is accompanied by the release of leptin. Recently, obesity was determined to be associated with various pulmonary diseases including asthma, acute lung injury, and chronic obstructive pulmonary disease. However, how obesity contributes to pulmonary diseases and whether leptin directly regulates lung inflammation remains unclear. We used cell and animal models to study the mechanisms of leptin mediation of pulmonary inflammation. We found that leptin activated de novo synthesis of cytosolic phospholipase A₂-α (cPLA₂-α) in vitro in the lung alveolar type II cells, A549, and in vivo in ICR mice. Upregulated cPLA₂-α protein was attenuated by pretreatment with an OB-R blocking antibody, U0126, SB202190, SP600125, Bay11-7086, garcinol, and p300 siRNA, suggesting roles of p42/p44 MAPK, p38 MAPK, JNK1/2, NF-κB, and p300 in leptin effects. Leptin enhanced the activities of p42/p44 MAPK, p38 MAPK, JNK1/2, and p65 NF-κB in a time-dependent manner. Additional studies have suggested the participation of OB-R, p42/p44 MAPK, and JNK1/2 in leptin-increased p65 phosphorylation. Furthermore, p300 phosphorylation and histone H4 acetylation were reduced by blockage of OB-R, p42/p44 MAPK, p38 MAPK, JNK1/2, and NF-κB in leptin-stimulated cells. Similarly, blockage of the MAPKs/NF-κB/p300 cascade significantly inhibited leptin-mediated cPLA₂-α mRNA expression. Our data as a whole showed that leptin contributed to lung cPLA₂-α expression through OB-R-dependent activation of the MAPKs/NF-κB/p300 cascade.
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