ArticleThe American journal of pathology2009
Lipopolysaccharide-induced epithelial monoamine oxidase mediates alveolar bone loss in a rat chronic wound model.
Article in The American journal of pathology, 2009. 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, 45 citations in OpenAlex.
- Topical selegiline accelerates cutaneous wound healing with phase-specific modulation of MAPK signaling.Inflammopharmacology · 2026Article
- MAO-A inhibition alleviates sepsis-driven lung injury via Nrf2/HO-1 pathway activation and suppression of pyroptosis.Journal of molecular histology · 2025Article
- Modulation of neuroimmune cytokine networks by antidepressants: implications in mood regulation.Translational psychiatry · 2025Review
- Cellular and molecular roles of reactive oxygen species in wound healing.Communications biology · 2024Review
- Serotonin Availability Shapes the Effects of Phenelzine on Inflammatory Response and Gene Expression in Macrophages.Cureus · 2024Article
- Deprenyl reduces inflammation during acute SIV infection.iScience · 2022Article
- Repurposing monoamine oxidase inhibitors (MAOI) for the treatment of rheumatoid arthritis possibly through modulating reactive oxidative stress mediated inflammatory cytokines.Inflammopharmacology · 2022Article
- Article
- MAO-A Inhibition by Metaxalone Reverts IL-1β-Induced Inflammatory Phenotype in Microglial Cells.International journal of molecular sciences · 2021Article
- Monoamine Oxidase-B Inhibitor Reduction in Pro-Inflammatory Cytokines Mediated by Inhibition of cAMP-PKA/EPAC Signaling.Frontiers in pharmacology · 2021Article
- Monoamine Oxidase Inhibitors: A Review of Their Anti-Inflammatory Therapeutic Potential and Mechanisms of Action.Frontiers in pharmacology · 2021Review
- Monoamine Oxidase-Related Vascular Oxidative Stress in Diseases Associated with Inflammatory Burden.Oxidative medicine and cellular longevity · 2019Review
- Visualization of Oxidative Stress Induced by Experimental Periodontitis in Keap1-Dependent Oxidative Stress Detector-Luciferase Mice.International journal of molecular sciences · 2016Article
- Wound healing by topical application of antioxidant iron chelators: kojic acid and deferiprone.International wound journal · 2013Article
- Immunomodulation Mechanism of Antidepressants: Interactions between Serotonin/Norepinephrine Balance and Th1/Th2 Balance.Current neuropharmacology · 2012Article
- Low-level diode laser therapy reduces lipopolysaccharide (LPS)-induced bone cell inflammation.Lasers in medical science · 2012Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) production is an antimicrobial response to pathogenic challenge that may, in the case of persistent infection, have deleterious effects on the tissue of origin. A rat periodontal disease model was used to study ROS-induced chronic epithelial inflammation and bone loss. Lipopolysaccharide (LPS) was applied for 8 weeks into the gingival sulcus, and histological analysis confirmed the onset of chronic disease. Junctional epithelium was collected from healthy and diseased animals using laser-capture microdissection, and expression microarray analysis was performed. Of 19,730 genes changed in disease, 42 were up-regulated >/=4-fold. Three of the top 10 LPS-induced genes, monoamine oxidase B (MAO/B) and flavin-containing monooxygenase 1 and 2, are implicated in ROS signaling. LPS-associated induction of the ROS mediator H(2)O(2), as well as MAO/B and tumor necrosis factor (TNF)-alpha levels were validated in the rat histological sections and a porcine junctional epithelial cell culture model. Topical MAO inhibitors significantly counteracted LPS-associated elevation of H(2)O(2) production and TNF-alpha expression in vivo and in vitro, inhibited disease-associated apical migration and proliferation of junctional epithelium and inhibited induced systemic H(2)O(2) levels and alveolar bone loss in vivo. These results suggest that LPS induces chronic wounds via elevated MAO/B-mediated increases in H(2)O(2) and TNF-alpha activity by epithelial cells and is further associated with more distant effects on systemic oxidative stress and alveolar bone loss.
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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.