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Participation of Ras and extracellular regulated kinase in the hyperplastic response of middle-ear mucosa during bacterial otitis media

Palacios, SD; Pak, K; Kayali, AG; Rivkin, AZ; Aletsee, C; Melhus, Åsa LU ; Webster, NJG and Ryan, AF (2002) In Journal of Infectious Diseases 186(12). p.1761-1769
Abstract
Hyperplasia of middle-ear mucosa (MEM) during otitis media (OM) is thought to be partially mediated by the actions of growth factors and their receptors. The intracellular pathway leading from the small G-protein Ras to the extracellular regulated kinases (Erks) often links growth factor stimulation to cellular proliferation. This study assessed whether this pathway is involved in MEM hyperplasia during bacterial OM via the activation of Erk1/Erk2 in MEM of an in vivo rat bacterial OM model. Activation was maximal at 1 and 6 h and at 1 week after introduction of bacteria into the middle ear. Additionally, an in vitro model of rat MEM in bacterial OM was treated with farnesyl transferase inhibitor 277 or the Mek inhibitor U0126. MEM... (More)
Hyperplasia of middle-ear mucosa (MEM) during otitis media (OM) is thought to be partially mediated by the actions of growth factors and their receptors. The intracellular pathway leading from the small G-protein Ras to the extracellular regulated kinases (Erks) often links growth factor stimulation to cellular proliferation. This study assessed whether this pathway is involved in MEM hyperplasia during bacterial OM via the activation of Erk1/Erk2 in MEM of an in vivo rat bacterial OM model. Activation was maximal at 1 and 6 h and at 1 week after introduction of bacteria into the middle ear. Additionally, an in vitro model of rat MEM in bacterial OM was treated with farnesyl transferase inhibitor 277 or the Mek inhibitor U0126. MEM explants treated with either inhibitor demonstrated significant suppression of bacterially induced growth. These data support a role for Ras and Erk signaling in MEM hyperplasia during bacterial OM. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Infectious Diseases
volume
186
issue
12
pages
1761 - 1769
publisher
Oxford University Press
external identifiers
  • wos:000179392800009
  • pmid:12447762
  • scopus:0037114939
ISSN
1537-6613
DOI
10.1086/345798
language
English
LU publication?
yes
id
1f31e0e4-5cd9-48fd-898f-e730a934c9c5 (old id 322801)
date added to LUP
2007-11-02 15:20:05
date last changed
2017-01-01 06:55:59
@article{1f31e0e4-5cd9-48fd-898f-e730a934c9c5,
  abstract     = {Hyperplasia of middle-ear mucosa (MEM) during otitis media (OM) is thought to be partially mediated by the actions of growth factors and their receptors. The intracellular pathway leading from the small G-protein Ras to the extracellular regulated kinases (Erks) often links growth factor stimulation to cellular proliferation. This study assessed whether this pathway is involved in MEM hyperplasia during bacterial OM via the activation of Erk1/Erk2 in MEM of an in vivo rat bacterial OM model. Activation was maximal at 1 and 6 h and at 1 week after introduction of bacteria into the middle ear. Additionally, an in vitro model of rat MEM in bacterial OM was treated with farnesyl transferase inhibitor 277 or the Mek inhibitor U0126. MEM explants treated with either inhibitor demonstrated significant suppression of bacterially induced growth. These data support a role for Ras and Erk signaling in MEM hyperplasia during bacterial OM.},
  author       = {Palacios, SD and Pak, K and Kayali, AG and Rivkin, AZ and Aletsee, C and Melhus, Åsa and Webster, NJG and Ryan, AF},
  issn         = {1537-6613},
  language     = {eng},
  number       = {12},
  pages        = {1761--1769},
  publisher    = {Oxford University Press},
  series       = {Journal of Infectious Diseases},
  title        = {Participation of Ras and extracellular regulated kinase in the hyperplastic response of middle-ear mucosa during bacterial otitis media},
  url          = {http://dx.doi.org/10.1086/345798},
  volume       = {186},
  year         = {2002},
}