Effect of the Absence of Heat Shock Protein 70.1 (hsp70.1) on Retinal Photic Injury

This study aimed to evaluate the protective effect of heat shock protein70 (hsp70) on retinal photic injuries, and to determine the relationship between hsp70s from hsp70.1 and 70.3. C57BL/6 wild type (hsp70.1+/+) and knockout type (hsp70.1-/-) mice from the same littermates were placed in light of 11000 lux for 6 hours, and were sacrificed at 1, 4, 7, and 14 days after stress. H & E staining, immunohistochemistry, and western blot analysis were performed. The hsp70.1-/- mice exhibited more disarranged and more diffusely destroyed photoreceptors than the hsp70.1+/+ mice. Hsp70 induction by light in both the hsp70.1 +/+ and hsp70.1 -/- mice peaked at 1 day after light stress. The Hsp70 level in the hsp70.1 +/+ mice reduced slowly and was almost constant for 7 days. However, in the hsp70.1 -/- mice, it decreased rapidly and returned, after 7 days, to a similar level to that prior to light exposure. According to which gene they originate from, hsp70s may play specific roles in protecting the retina against stresses. Hsp70 from the hsp70.1 gene may act as a sustained responder to retinal photic injury.