Cellular senescence involves an intracrine prostaglandin E2 pathway in human fibroblasts
Abstract
Cyclooxygenase 2 and release of prostaglandin E2 are involved in many responses including inflammation and are upregulated during cellular senescence. However, little is known about the role of lipid inflammatory mediators in senescence. Here, we investigated the mechanism by which the COX-2/PGE2 axis induces senescence. Using the NS398 specific inhibitor of COX-2, we provide evidence that reactive oxygen species by-produced by the COX-2 enzymatic activity are negligible in front of the total senescence-associated oxidative stress. We therefore investigated the role of PGE2 by invalidating the PGE2 synthases downstream of COX-2, or the specific PGE2 receptors, or by applying PGE2 or specific agonists or antagonists. We evaluated the effect on senescence by evaluating the senescence-associated proliferation arrest, the percentage of senescence-associated beta-galactosidase-positive cells, and the expression of senescent molecular markers such as IL-6 and MCP1. We show that PGE2 acting on its EP specific receptors is able to induce both the onset of senescence and the maintenance of the phenotype. It did so only when the PGE2/lactate transporter activity was enhanced, indicating that PGE2 acts on senescence more via the pool of intracellular EP receptors than via those localized at the cell surface. Treatment with agonists, antagonists and silencing of the EP receptors by siRNA revealed that EP3 was the most involved in transducing the intracrine effects of PGE2. Immunofluorescence experiments confirmed that EP3 was more localized in the cytoplasm than at the cell surface. Taken together, these results suggest that COX-2 contributes to the establishment and maintenance of senescence of normal human fibroblasts via an independent-ROS and a dependent-PGE2/EPs intracrine pathway.
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PGD2 and PGJ2 have similar effects on senescence phenotypes, and PGE2 has similar effects to a lesser degree.
“PGD2 and PGJ2 had similar effects on senescence phenotypes (Figures S4G–S4L), as did PGE2 to a lesser degree, as reported (Martien et al., 2013).”
From Oxylipin biosynthesis reinforces cellular senescence and allows detection of senolysis (2021) · cites this paper as Martien et al., 2013
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Phosphoproteome Dynamics in Onset and Maintenance of Oncogene-induced Senescence
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- Authors
- Martien, S., Pluquet, O., Vercamer, C., Malaquin, N., Martin, N., Gosselin, K., Pourtier, A., & Abbadie, C.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Abbadie, Corinne
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
- Publisher
- Elsevier BV
- Published
- 2013-07
- Volume
- 1831
- Issue
- 7
- Pages
- 1217-1227
- ISSN
- 1388-1981 (ISSN-L)
- OpenAlex
- W2003652428
- Cited by
- 50
- References
- 64
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 5 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 5 · 2016: 7 · 2015: 2 · 2014: 4
- FWCI
- 3.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Association pour la Recherche sur le Cancer (ARC)
- Ligue contre le Cancer
- Conseil Régional Nord/Pas-de-Calais
- European Regional Development Fund
- Ministry of Research
- Fondation pour la Recherche Médicale (FRM)
- Institut Pasteur de Lille
- Région NPdC
- Société Française du Cancer
- University of Lille 2
- Centre National de la Recherche Scientifique (CNRS)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, prostaglandin E2, cyclooxygenase-2, EP3 receptor, intracrine signaling, human fibroblasts, lactate transporters, senescence-associated β-galactosidase, interleukin-6, MCP-1, reactive oxygen species, PGE2 receptors
- MeSH terms
- Cell Line, Fibroblasts, Humans, Dinoprostone, Signal Transduction, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Dermis, Cyclooxygenase 2, Receptors, Prostaglandin E, EP2 Subtype, Receptors, Prostaglandin E, EP3 Subtype
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