April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Deleterious Role of Anti-High Mobility Group Box 1 Monoclonal Antibody in Retinal Ischemia-Reperfusion Injury
Author Affiliations & Notes
  • K. Hirooka
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • H. Yang
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
    Ophthalmology, Shengjing Affiliated Hospital, China Medical University, Shenyang, China
  • K. Fukuda
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • M. Mizote
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • F. Shiraga
    Ophthalmology, Kagawa Univ Faculty of Medicine, Kita-gun, Japan
  • Footnotes
    Commercial Relationships  K. Hirooka, None; H. Yang, None; K. Fukuda, None; M. Mizote, None; F. Shiraga, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4698. doi:
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      K. Hirooka, H. Yang, K. Fukuda, M. Mizote, F. Shiraga; Deleterious Role of Anti-High Mobility Group Box 1 Monoclonal Antibody in Retinal Ischemia-Reperfusion Injury. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4698.

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Abstract

Purpose: : To investigate the effect of anti-high mobility group box 1 (HMGB1) monoclonal antibody (mAb) against ischemia reperfusion injury in the rat retina.

Methods: : Retinal ischemia was induced by increasing intraocular pressure to 130 mmHg and maintaining that level for 45 minutes. An intraperitoneal injection of HMGB1 was administered 30 min before ischemia. At 7 days after the ischemia, retinal damage was evaluated. Immunohistochemistry and image analysis were used to measure changes in the levels of reactive oxygen species (ROS) and the localization of anti-HMGB1 mAb. Dark-adapted full-field electroretinography (ERG) was also performed.

Results: : Pretreatment with anti-HMGB1 mAb significantly enhanced the ischemic injury of the inner retina. Anti-HMGB1 mAb expression increased at 6 to 12 hours after ischemia in the inner retina. After the ischemia, production of ROS was detected in retinal cells. However, pretreatment with anti-HMGB1 mAb increased the production of ROS. On the seventh postoperative day, the amplitudes of the ERG b-waves were significantly higher in the vehicle group than in the groups pretreated with anti-HMGB1 mAb.

Conclusions: : Anti-HMGB1 mAb plays a large deleterious role in ischemia-reperfusion injury in an in vivo model of retinal injury. Anti-HMGB1 mAb function should be further explored to develop neuroprotective therapeutic strategies for acute retinal ischemic disorders.

Keywords: ischemia • oxidation/oxidative or free radical damage • electroretinography: non-clinical 
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