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

Sean D Palacios1, Kwang Pak, Ayse G Kayali

  • 1Department of Head and Neck Surgery, University of California, San Diego, School of Medicine, La Jolla, California, USA.

The Journal of Infectious Diseases
|November 26, 2002
PubMed

Insights

Bacterial otitis media (OM) causes middle-ear mucosa (MEM) hyperplasia. Ras and Erk signaling pathways are involved in this growth, as inhibiting them suppressed bacterial-induced MEM growth in rats.

Area of Science:

  • Otolaryngology
  • Molecular Biology
  • Cellular Biology

Background:

  • Middle-ear mucosa (MEM) hyperplasia is a hallmark of otitis media (OM).
  • Growth factors and their signaling pathways are implicated in mediating this hyperplasia.
  • The Ras-Erk intracellular signaling cascade is a key pathway linking growth factor stimulation to cellular proliferation.

Purpose of the Study:

  • To investigate the involvement of the Ras-Erk signaling pathway in MEM hyperplasia during bacterial OM.
  • To assess the activation of Erk1/Erk2 in MEM during an in vivo rat model of bacterial OM.

Main Methods:

  • An in vivo rat model of bacterial OM was utilized.
  • Erk1/Erk2 activation in MEM was measured at various time points post-bacterial introduction.
  • An in vitro model using rat MEM explants was treated with farnesyl transferase inhibitor 277 or Mek inhibitor U0126.

Main Results:

  • Erk1/Erk2 activation in MEM was maximal at 1 and 6 hours, and 1 week after bacterial inoculation.
  • Treatment of MEM explants with farnesyl transferase inhibitor 277 or Mek inhibitor U0126 significantly suppressed bacterially induced growth.

Conclusions:

  • The Ras-Erk signaling pathway plays a significant role in MEM hyperplasia during bacterial OM.
  • Inhibiting key components of this pathway can suppress bacterial-induced MEM growth, suggesting potential therapeutic targets.

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