May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
17ß–Estradiol Exerts a Neuroprotective Effect Through Phosphorylation of ERK in NMDA–Induced Retinal Damage
Author Affiliations & Notes
  • Y. Hayashi
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Ophthalmology,
  • R. Ohtani–Kaneko
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Anatomy and Cell Biology,
  • Y. Kitaoka
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Ophthalmology,
  • Y. Munemasa
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Ophthalmology,
  • K. Kuribayashi
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Ophthalmology,
  • J. Kogo
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Pharmacology,
  • H. Takeda
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Ophthalmology,
  • K. Hirata
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Anatomy and Cell Biology,
  • S. Ueno
    St.Mariannna Univ Sch Med, Kawasaki–shi, Japan
    Ophthalmology,
  • Footnotes
    Commercial Relationships  Y. Hayashi, None; R. Ohtani–Kaneko, None; Y. Kitaoka, None; Y. Munemasa, None; K. Kuribayashi, None; J. Kogo, None; H. Takeda, None; K. Hirata, None; S. Ueno, None.
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 2582. doi:
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      Y. Hayashi, R. Ohtani–Kaneko, Y. Kitaoka, Y. Munemasa, K. Kuribayashi, J. Kogo, H. Takeda, K. Hirata, S. Ueno; 17ß–Estradiol Exerts a Neuroprotective Effect Through Phosphorylation of ERK in NMDA–Induced Retinal Damage . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2582.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To investigate whether extracellular signal–regulated kinase (ERK) is involved in the neuroprotective effect of 17ß–estradiol in NMDA–induced retinal neurotoxicity.

Methods: : Eight–week–old female Wistar rats were used as subjects. All subjects were divided into sham operated and ovariectomized (OVX) groups. The OVX rats were treated with either solvent vehicle or 17ß–estradiol subcutaneous implant immediately after ovariectomy. At 2 weeks post–operation, the rats were received intravitreal injection of NMDA with or without U 0126 (ERK–inhibitor) or ICI 182,780 (estrogen receptor inhibitor) . The eyes were enucleated at 6, 12 hours or 7 days after injection. Expression of p–ERK was examined by Western blot analysis at 6 hours and 7 days after intravitreal injection. The effects of 17ß–estradiol on NMDA treated retina were evaluated by TUNEL study 12 hours after injection and by Hematoxylin and Eosin (HE) staining 7 days after injection. Moreover, the effect of U 0126 or ICI 182,780 on protective effect of 17ß–estradiol was evaluated in Fluorogold labeled RGCs number.

Results: : 17ß–estradiol has an antiapoptotic effect evaluated by TUNEL. 17ß–estradiol preserved inner retina as shown by HE staining. Fluorogold retrograde labeling also showed the neuroprotective effect of 17ß–estradiol on RCGs. These protective effects of 17ß–estradiol were suppressed by co–injection of U 0126 or ICI 182,780. Western blot analysis showed that 17ß–estradiol increased p–ERK protein levels and this increase was inhibited by co–injection of U 0126 or ICI 182,780.

Conclusions: : These findings suggest that 17ß–estradiol has a neuroprotective effect through phosphorylation of ERK in retina.

Keywords: apoptosis/cell death • retina • ganglion cells 
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