Altered expression and signalling of EP2 receptor in nasal polyps of AERD patients: role in inflammation and remodelling
| Autor: | César Picado, Laura Pujols, J. Roca-Ferrer, Maria Perez-Gonzalez, J Mullol, R Torres, L Machado-Carvalho, Isam Alobid |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Prostaglandin E2 receptor Respiratory Tract Diseases Down-Regulation Prostaglandin Mucous membrane of nose Inflammation Stimulation Dinoprostone 03 medical and health sciences chemistry.chemical_compound Nasal Polyps 0302 clinical medicine Internal medicine Cyclic AMP Humans Receptors Prostaglandin E Medicine Nasal polyps Alprostadil Receptor Cell Proliferation Aspirin business.industry Anti-Inflammatory Agents Non-Steroidal Granulocyte-Macrophage Colony-Stimulating Factor General Medicine Fibroblasts Middle Aged medicine.disease Nasal Mucosa 030104 developmental biology Endocrinology 030228 respiratory system Otorhinolaryngology chemistry Disease Progression Female lipids (amino acids peptides and proteins) Signal transduction medicine.symptom business Signal Transduction |
| Zdroj: | Rhinology journal. 54:254-265 |
| ISSN: | 0300-0729 |
| DOI: | 10.4193/rhin15.207 |
| Popis: | Background: Down-regulation of the E-prostanoid (EP)2 receptor has been reported in aspirin exacerbated respiratory disease (AERD). We aimed to evaluate the expression and activation of EP receptors in AERD and their role in prostaglandin (PG) E2 signalling. Methods: Samples were obtained from nasal mucosa of control subjects (NM-C, n=7) and from nasal polyps of AERD patients (NP-AERD, n=7). Expression of EP1-4 was assessed at baseline. Fibroblasts were stimulated with receptor agonists to measure cAMP levels, cell proliferation and granulocyte-macrophage colony-stimulating factor (GM-CSF) release. Results: NM-C and NP-AERD samples and fibroblasts expressed EP2, EP3 and EP4 at baseline. Lower expression of EP2 and higher expression of EP4 was observed in NP-AERD compared with NM-C. Stimulation with PGE2 and butaprost caused a higher increase in cAMP in NM-C than in NP-AERD. On the contrary, CAY10598 produced a higher production of cAMP in NP-AERD compared with NM-C. The anti-proliferative effect of PGE2 and butaprost was lower in NP-AERD than in NM-C fibroblasts. Similarly, the capacity of PGE2 and butaprost to inhibit GM-CSF release was lower in NP-AERD than in NM-C. Conclusions: The altered expression of EP2 in AERD may contribute to reduce the capacity of PGE2 to mediate anti-proliferative and anti-inflammatory effects. |
| Databáze: | OpenAIRE |
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