Korean J Ophthalmol.  2005 Jun;19(2):116-121. 10.3341/kjo.2005.19.2.116.

Protective Effect of Heat Shock Proteins 70.1 and 70.3 on Retinal Photic Injury after Systemic Hyperthermia

• Kim JH
• Kim JH
• Yu YS
• Jeong SM
• Kim KW

• KMID: 754408
• DOI: http://doi.org/10.3341/kjo.2005.19.2.116

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.

Keyword

Hsp70.1; Hsp70.3; Hyperthermia; Retinal photic injury

MeSH Terms

Animals
Female
Fever/metabolism/*physiopathology
Heat-Shock Proteins 70/*metabolism
In Vitro
Light/*adverse effects
Mice
Mice, Inbred C57BL
Radiation Injuries/*prevention & control
Research Support, Non-U.S. Gov't
Retina/*radiation effects