Signaling pathways in interleukin-1beta-mediated middle ear mucin secretion. Laryngoscope 2006 Feb;116(2):207-11
Date
02/10/2006Pubmed ID
16467705DOI
10.1097/01.mlg.0000191467.63650.9eScopus ID
2-s2.0-33645765306 (requires institutional sign-in at Scopus site) 7 CitationsAbstract
OBJECTIVES: The objectives of this study were to investigate the role of the phosphatidylcholine-specific phospholipase C (PC-PLC), protein kinase C (PKC), and nitric oxide synthase (NOS) pathways during upregulation of mucin secretion by middle ear epithelium after exposure to interleukin-1beta and to examine the ability of a specific interleukin-1 receptor antagonist (IL-1betara) to block this increased secretion.
MATERIALS AND METHODS: Primary chinchilla middle ear epithelial cultures were established and exposed to IL-1beta. Specific inhibitors of calmodulin, PC-PLC, PKC, and NOS pathways were used to investigate the potential role of these pathways leading to increased epithelial mucin secretion after exposure to IL-1beta. Mucin secretion was characterized by exclusion chromatography and liquid scintillation.
RESULTS: Epithelial cultures exposed to IL-1beta demonstrate an increase in mucin secretion that is blocked by specific inhibitors of PC-PLC, PKC, and NOS, but not by inhibitors of calmodulin. In addition, mucin secretion stimulated by IL-1beta was reversible with use of a specific IL-1betara.
CONCLUSIONS: IL-1beta stimulates mucin secretion from middle ear epithelium and its effects can be reversed by IL-1betara. PC-PLC, PKC, and NOS pathways play a role in the increased secretion of mucin in middle ear epithelial cells after exposure to IL-1beta.
Author List
Kerschner JE, Yang C, Burrows A, Cioffi JAAuthor
Joseph E. Kerschner MD Provost, Executive Vice President, Dean, Professor in the School of Medicine Administration department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsCalmodulin
Cell Proliferation
Cell Survival
Cells, Cultured
Chinchilla
Ear, Middle
Interleukin-1
Mucins
Nitric Oxide Synthase
Protein Kinase C
Receptors, Interleukin-1
Signal Transduction
Type C Phospholipases
Up-Regulation