Protective Effect of Heat Shock Proteins 70.1 and 70.3 on Retinal Photic Injury after Systemic Hyperthermia. |
Jin Hyoung Kim, Jeong Hun Kim, Young Suk Yu, Seon Mi Jeong, Kyu Won Kim |
1Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Korea. 2Seoul Artificial Eye Center and Clinical Research Institute, Seoul National University Hospital, Seoul, Korea. ysyu@snu.ac.kr 3Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea. |
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Abstract |
PURPOSE This study aimed to determine the relationship between the heat shock protein 70 from hsps70.1 and 70.3 on retinal photic injury after systemic hyperthermia. METHODS: Eight-week-old female C57BL/6 mice were kept at a constant temperature of 41~42 degrees C for 25~30 minutes. After dark-adaptation for 8 hours, intense light of 11000 lux was maintained for 6 hours. Histology and immunohistochemistry for the inducible heat shock protein 70 (hsp70), the constitutive heat shock protein 70 (hsc70), and western blot analysis, reverse transcriptase-polymerase chain reaction for hsp70.1 and hsp70.3 were performed just before photic injury and after 1, 4, 7, and 14 days. RESULTS: Light-induced retinal degeneration was prevented by thermotolerance. After hyperthermia, hsp70 was densely expressed in the inner segment of the photoreceptor layer on the photic injury. Hsp70 expression increased for 4 days after photic injury and slowly decreased thereafter. mRNA from hsp70.3 was induced earlier than that of hsp70.1. CONCLUSIONS: Retinal photic injury was prevented by hyperthermia-induced hsp70. Hsp70 from hsp70.3 may be a rapid and short-lived responder, and that from hsp70.1 is a slower and more sustained responder. Hsp70 from hsp70.3 may be an initial retinal chaperone while hsp70 from hsp70.1 may be a sustained chaperone. |
Key Words:
Hsp70.1;Hsp70.3;Hyperthermia;Retinal photic injury |
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