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Phosphorylation of extracellular signal-regulated kinase and p27(KIP1) after retinal detachment

Satoru Kase1, Kazuhiko Yoshida, Takayuki Harada

  • 1Department of Ophthalmology and Visual Sciences, Hokkaido University Graduate School of Medicine, N15 W7, Kita-ku, Sapporo, 060-8638, Japan.

Graefe'S Archive for Clinical and Experimental Ophthalmology = Albrecht Von Graefes Archiv Fur Klinische Und Experimentelle Ophthalmologie
|August 3, 2005
PubMed
Abstract

Insights

Retinal detachment triggers Müller cell proliferation via the ERK pathway, affecting p27(KIP1) and cyclin D1 expression. Inhibiting ERK signaling modulates these changes, impacting cell cycle progression.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Biology

Background:

  • Müller glial cells play crucial roles in retinal structure and function.
  • Retinal detachment can lead to Müller cell activation and proliferation.
  • The extracellular signal-regulated kinase (ERK) pathway is implicated in cellular responses to injury.

Purpose of the Study:

  • To investigate the role of the ERK pathway in Müller cell proliferation following retinal detachment.
  • To examine the impact of ERK signaling on the expression and phosphorylation of p27(KIP1) and the expression of cyclin D1.
  • To determine the effect of ERK inhibition on these molecular events and proliferation.

Main Methods:

  • Immunohistochemistry was used to detect phosphorylated ERK1/2 (pERK1/2), p27(KIP1), S10-phospho-p27, cyclin D1, and PCNA in mouse retinas post-detachment.
  • An ERK inhibitor (PD98059) was administered to assess its effects on molecular markers and proliferation.
  • Western blotting analyzed p27(KIP1) and cyclin D1 expression in isolated mouse Müller cells treated with bFGF and PD98059.

Main Results:

  • Following retinal detachment, pERK1/2, p27(KIP1), and S10-phospho-p27 were upregulated in the inner nuclear layer (INL).
  • PD98059 treatment inhibited pERK1/2 and S10-phospho-p27 expression, and also suppressed cyclin D1 induction and PCNA expression.
  • bFGF exposure decreased p27(KIP1) and increased cyclin D1 in Müller cells, effects reversed by PD98059.

Conclusions:

  • ERK pathway activation is critical for Müller cell proliferation after retinal detachment.
  • The expression of p27(KIP1) and cyclin D1 are key downstream events regulated by ERK signaling in this context.
  • Targeting the ERK pathway may offer therapeutic potential for managing retinal injury-induced Müller cell responses.

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