Tags

Type your tag names separated by a space and hit enter

Deleterious role of anti-high mobility group box 1 monoclonal antibody in retinal ischemia-reperfusion injury.
Curr Eye Res. 2011 Nov; 36(11):1037-46.CE

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.

MATERIALS AND METHODS

Retinal ischemia was induced by increasing and then maintaining intraocular pressure at 130 mmHg for 45 min. An intraperitoneal injection of anti-HMGB1 mAb was administered 30 min before ischemia. Retinal damage was evaluated at 7 days after the ischemia. 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 retina. HMGB1 expression increased at 6-12 h after ischemia in the 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 both the ERG a- and b-waves were significantly higher in the vehicle group than in the groups pretreated with anti-HMGB1 mAb.

CONCLUSIONS

The current in vivo model of retinal injury demonstrated that anti-HMGB1 mAb plays a large deleterious role in ischemia-reperfusion injury. In order to develop neuroprotective therapeutic strategies for acute retinal ischemic disorders, further studies on anti-HMGB1 mAb function are needed.

Authors+Show Affiliations

Department of Ophthalmology, Kagawa University, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21999229

Citation

Yang, Hongwei, et al. "Deleterious Role of Anti-high Mobility Group Box 1 Monoclonal Antibody in Retinal Ischemia-reperfusion Injury." Current Eye Research, vol. 36, no. 11, 2011, pp. 1037-46.
Yang H, Yang S, Hirooka K, et al. Deleterious role of anti-high mobility group box 1 monoclonal antibody in retinal ischemia-reperfusion injury. Curr Eye Res. 2011;36(11):1037-46.
Yang, H., Yang, S., Hirooka, K., Liu, Y., Fujita, T., Fukuda, K., Nakamutra, T., Itano, T., Zhang, J., Nishibori, M., & Shiraga, F. (2011). Deleterious role of anti-high mobility group box 1 monoclonal antibody in retinal ischemia-reperfusion injury. Current Eye Research, 36(11), 1037-46. https://doi.org/10.3109/02713683.2011.594201
Yang H, et al. Deleterious Role of Anti-high Mobility Group Box 1 Monoclonal Antibody in Retinal Ischemia-reperfusion Injury. Curr Eye Res. 2011;36(11):1037-46. PubMed PMID: 21999229.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Deleterious role of anti-high mobility group box 1 monoclonal antibody in retinal ischemia-reperfusion injury. AU - Yang,Hongwei, AU - Yang,Shenyang, AU - Hirooka,Kazuyuki, AU - Liu,Ye, AU - Fujita,Tomoyoshi, AU - Fukuda,Kouki, AU - Nakamutra,Takehiro, AU - Itano,Toshifumi, AU - Zhang,Jiyong, AU - Nishibori,Masahiro, AU - Shiraga,Fumio, PY - 2011/10/18/entrez PY - 2011/10/18/pubmed PY - 2012/2/15/medline SP - 1037 EP - 46 JF - Current eye research JO - Curr Eye Res VL - 36 IS - 11 N2 - PURPOSE: To investigate the effect of anti-high mobility group box 1 (HMGB1) monoclonal antibody (mAb) against ischemia-reperfusion injury in the rat retina. MATERIALS AND METHODS: Retinal ischemia was induced by increasing and then maintaining intraocular pressure at 130 mmHg for 45 min. An intraperitoneal injection of anti-HMGB1 mAb was administered 30 min before ischemia. Retinal damage was evaluated at 7 days after the ischemia. 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 retina. HMGB1 expression increased at 6-12 h after ischemia in the 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 both the ERG a- and b-waves were significantly higher in the vehicle group than in the groups pretreated with anti-HMGB1 mAb. CONCLUSIONS: The current in vivo model of retinal injury demonstrated that anti-HMGB1 mAb plays a large deleterious role in ischemia-reperfusion injury. In order to develop neuroprotective therapeutic strategies for acute retinal ischemic disorders, further studies on anti-HMGB1 mAb function are needed. SN - 1460-2202 UR - https://www.unboundmedicine.com/medline/citation/21999229/Deleterious_role_of_anti_high_mobility_group_box_1_monoclonal_antibody_in_retinal_ischemia_reperfusion_injury_ L2 - https://www.tandfonline.com/doi/full/10.3109/02713683.2011.594201 DB - PRIME DP - Unbound Medicine ER -