Impaired E Prostanoid2 Expression and Resistance to Prostaglandin E2 in Nasal Polyp Fibroblasts from Subjects with Aspirin-Exacerbated Respiratory Disease

• Published in: American journal of respiratory cell and molecular biology Vol. 54; no. 1; pp. 34 - 40
• Main Authors: Cahill, Katherine N, Raby, Benjamin A, Zhou, Xiaobo, Guo, Feng, Thibault, Derek, Baccarelli, Andreas, Byun, Hyang-Min, Bhattacharyya, Neil, Steinke, John W, Boyce, Joshua A, Laidlaw, Tanya M
• Format: Journal Article
• Language: English
• Published: United States American Thoracic Society 01.01.2016
• Subjects: Acetylation; Adult; Asthma, Aspirin-Induced - genetics; Asthma, Aspirin-Induced - metabolism; Asthma, Aspirin-Induced - pathology; Boston; Case-Control Studies; Cell Proliferation - drug effects; Cells, Cultured; Dinoprostone - analogs & derivatives; Dinoprostone - metabolism; Dinoprostone - pharmacology; DNA Methylation - drug effects; Dose-Response Relationship, Drug; Epigenesis, Genetic - drug effects; Female; Fibroblasts - drug effects; Fibroblasts - metabolism; Fibroblasts - pathology; Gene Expression Regulation; Histone Deacetylase Inhibitors - pharmacology; Histones - metabolism; Humans; Male; Middle Aged; Nasal Polyps - genetics; Nasal Polyps - metabolism; Nasal Polyps - pathology; Original Research; Promoter Regions, Genetic; Receptors, Prostaglandin E, EP2 Subtype - agonists; Receptors, Prostaglandin E, EP2 Subtype - genetics; Receptors, Prostaglandin E, EP2 Subtype - metabolism; RNA, Messenger - genetics; RNA, Messenger - metabolism; Signal Transduction; Virginia; Virginia; Boston; DNA methylation; prostaglandin E2; histone acetylation; E prostanoid type 2 receptor; aspirin-exacerbated respiratory disease

Recurrent, rapidly growing nasal polyps are hallmarks of aspirin-exacerbated respiratory disease (AERD), although the mechanisms of polyp growth have not been identified. Fibroblasts are intimately involved in tissue remodeling, and the growth of fibroblasts is suppressed by prostaglandin E2 (PGE2),...