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Morphological Analyses on Retinal Glial Responses to Glaucomatous Injury Evoked by Venous Cauterization

  • Lee, Ji-Yeon (Department of Anatomy, College of Medicine, The Catholic University of Korea) ;
  • Shin, Ji-Man (Department of Anatomy, College of Medicine, The Catholic University of Korea) ;
  • Chun, Myung-Hoon (Department of Anatomy, College of Medicine, The Catholic University of Korea) ;
  • Oh, Su-Ja (Department of Anatomy, College of Medicine, The Catholic University of Korea)
  • Received : 2014.03.20
  • Accepted : 2014.03.27
  • Published : 2014.03.30

Abstract

Retinal glial responses to hypertensive glaucomatous injury were spatiotemporally surveyed. Retinas as a whole or vertical sections were processed for anti-glial fibrillary acidic protein (GFAP), anti-Iba1, anti-nerve growth factor (NGF), and anti-tumor necrosis factor (TNF)-${\alpha}$ immunohistochemistry for confocal microscopic analyses. The optic nerve head of paired controls was processed for electron microscopy. GFAP positive astrocytes appeared in the nerve fiber layer in the glaucomatous and control retinas, changing from fine protoplasmic to stout fibrous parallel to glaucomatous duration. Iba1 positive microglia appeared in both retinas, and enormous reaction appeared at the latest glaucomatous. M$\ddot{u}$ller reaction detected by GFAP reactivity expanded from the end feet to whole profile following to duration in the glaucomatous. NGF reactivity expended from the end feet to the proximal radial processes of the M$\ddot{u}$ller cells in both retinas according to glaucomatous duration. TNF-${\alpha}$ immunoreactivity in the nerve fiber layer was stronger in both the glaucomatous and controls than in the normal, and exceptionally at the latest glaucomatous was even lower than the normal. The astrocytes in the optic nerve head are interconnected with each other via gap junction. These results demonstrate that astrocyte reaction propagates to the contralateral via physical links, and TNF-${\alpha}$ is correlated with NGF production for neuroprotection in response to hypertensive glaucomatous injury.

Keywords

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