Hyperthermia Protects Against Light Damage in the Rat Retina

Barbe, Mary F.; Tytell, Michael; Gower, David J.; Welch, William J.

doi:10.1126/science.3175623

Cited by 402 publications

(175 citation statements)

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“…The phenomenon of induced tolerance was also observed in in vivo mammalian cells. Barbe et al (1988) made rats hy perthermic and showed that the retina was less sen sitive to light damage compared to untreated con trols. This change was correlated to protein synthe sis in the retina after hyperthermia.…”

Section: Discussionmentioning

confidence: 99%

Induced Tolerance to Ischemia in Gerbil Hippocampal Neurons

Kirino

Tsujita

Tamura

1991

J Cereb Blood Flow Metab

565

216

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Summary: Brief ischemia induced tolerance to subse quent ischemia in the hippocampal neurons. Male Mon golian gerbils were subjected to 2 min of ischemia in an awake condition. This ischemic insult only rarely pro duced neuronal damage in the gerbil brain. One day (n = 9), 2 days (n = 9), or 4 days (n = 10) following the first brief ischemia, the animals (double-ischemia group) were subjected to the second ischemia for 5 min. The single ischemia group received a sham procedure instead of the first ischemia and was identically subjected to the second ischemia I day (n = 9), 2 days (n = 10), and 4 days (n = 13) following the sham procedure. One week following the second ischemia, all gerbils were perfusion fixed and the neuronal density in the hippocampal CA I sector was measured. In double-ischemia groups, the neuronal denThe brain is particularly vulnerable to distur bances of energy metabolism, such as ischemia, an oxia, hypoglycemia, or status epilepticus (Auer and Siesj6, 1988; Siesj6 and Bengtsson, 1989). Even a brief episode of ischemia destroys certain groups of ischemia-sensitive neurons. These selectively vul nerable neurons are found in the hippocampal CA 1 sector, in the dorsolateral striatum, in certain layers of the cerebral cortex, and in the cerebellar cortex (Wieloch, 1985). Among these vulnerable cells in the brain, hippocampal CAl pyramidal cells have been the most extensively studied. Following brief ischemia, CA 1 pyramidal cells recover energy me tabolism (Pulsinelli and Duffy, 1983; Arai et a!. , 1986) and electrophysiological activity (Suzuki et a!., 1983). The fine structure of CA 1 pyramidal cells is maintained well until they are disintegrated 3 or 4Received July 18 , 1990 ; revised August 27 , 1990 ; accepted Au gust 31 , 1990 .Ad dress correspondence and reprint requests to Dr . T . Kirino at Department of Neurosurgery , Teikyo University School of Medicine , 7-3-\ Kaga , It abashi-ku , Tokyo 173 , Japan .Abbreviation used: hsp70 , 70-kDa heat-shock protein . 299sity per I-mm length of the pyramidal cell layer was 103.4 ± 93. 1 (SD) in the I-day subgroup, 125. 6 ± 64. 2 in the 2-day subgroup, and 176. 2 ± 93.7 in the 4-day subgroup, while the density in normal gerbils was 254.7 ± 18.6. The average neuronal density in the single-ischemia group was much lower than that in the double-ischemia group (whole control group: 10. 9 ± 27.4). Immunostaining using monoclonal antibody raised against 70-kDa heat-shock protein revealed an increase in 70-kDa heat-shock protein in the CAl area following 2 min of ischemia. Very brief ischemia induces heat-shock proteins and, presumably, thereby renders neurons more tolerant to subsequent metabolic stress.

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Section: Discussionmentioning

confidence: 99%

Induced Tolerance to Ischemia in Gerbil Hippocampal Neurons

Kirino

Tsujita

Tamura

1991

J Cereb Blood Flow Metab

565

216

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“…For example, short-term total body heat-stress has been shown to prevent light-induced damage to the photoreceptors in the retina, ischemia-induced death of hippocampal neurons and cardiac myocytes, carbon tetrachlorideinduced hepatotoxicity, and lipopolysaccharideinduced pulmonary fibrosis (Barbe et al 1988;Chopp et al 1989;Marber et al 1993;Hagiwara et al 2007). In the auditory system, total body heat stress is protective against noise-induced hearing loss (Yoshida et al 1999).…”

Section: Figmentioning

confidence: 99%

Hsp70 Inhibits Aminoglycoside-Induced Hair Cell Death and is Necessary for the Protective Effect of Heat Shock

Taleb

Brandon

Lee

et al. 2008

JARO

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Sensory hair cells of the inner ear are sensitive to death from aging, noise trauma, and ototoxic drugs. Ototoxic drugs include the aminoglycoside antibiotics and the antineoplastic agent cisplatin. Exposure to aminoglycosides results in hair cell death that is mediated by specific apoptotic proteins, including cJun N-terminal kinase (JNK) and caspases. Induction of heat shock proteins (Hsps) is a highly conserved stress response that can inhibit JNK-and caspasedependent apoptosis in a variety of systems. We have previously shown that heat shock results in a robust upregulation of Hsps in the hair cells of the adult mouse utricle in vitro. In addition, heat shock results in significant inhibition of both cisplatin-and aminoglycoside-induced hair cell death. In our system, Hsp70 is the most strongly induced Hsp, which is upregulated over 250-fold at the level of mRNA 2 h after heat shock. Therefore, we have begun to examine the role of Hsp70 in mediating the protective effect of heat shock. To determine whether Hsp70 is necessary for the protective effect of heat shock against aminoglycoside-induced hair cell death, we utilized utricles from Hsp70.1/3 −/− mice. While heat shock inhibited gentamicin-induced hair cell death in wild-type utricles, utricles from Hsp70.1/3 −/− mice were not protected. In addition, we have examined the role of the major heat shock transcription factor, Hsf1, in mediating the protective effect of heat shock. Utricles from Hsf1 −/− mice and wild-type littermates were exposed to heat shock followed by gentamicin. The protective effect of heat shock on aminoglycoside-induced hair cell death was only observed in wildtype mice and not in Hsf1 −/− mice. To determine whether Hsp70 is sufficient to protect hair cells, we have utilized transgenic mice that constitutively overexpress Hsp70. Utricles from Hsp70-overexpressing mice and wild-type littermates were cultured in the presence of varying neomycin concentrations for 24 h. The Hsp70-overexpressing utricles were significantly protected against neomycin-induced hair cell death at moderate to high doses of neomycin. This protective effect was achieved without a heat shock. Taken together, these data indicate that Hsp70 and Hsf1 are each necessary for the protective effect of heat shock against aminoglycoside-induced death. Furthermore, overexpression of Hsp70 alone significantly inhibits aminoglycoside-induced hair cell death.

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“…Heat shock proteins have been proven to play a key role in protecting stressed cell and organisms, and preventing or reversing disorders caused by stress (Barbe et al, 1988). The protein acts as a molecular chaperone by binding to other cellular proteins, assisting intracellular transport, and folding into the proper secondary structures and thus, preventing aggregation of protein during stress (Chirico et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

A note on heat shock protein 70 expression in goats subjected to road transportation under hot, humid tropical conditions

Zulkifli

Norbaiyah

Yoke-Kqueen

et al. 2010

Animal

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The influence of two different stocking densities (0.20 m 2 /animal and 0.40 m 2 /animal) in transit under the hot, humid tropical conditions on heat shock protein (hsp) 70 induction was investigated in 60 Boer does. The animals were road transported for 3 h and the control group was kept under normal conditions in the farm. Irrespective of stocking density, transportation significantly increased hsp 70 densities ( P , 0.05) in the kidneys. The hsp 70 response in the kidneys was more profound compared with those of heart tissues. Higher stocking density was more stressful to the goats based on hsp 70 expression. These results suggest that, irrespective of stocking density, transportation under hot, humid tropical conditions evoked hsp 70 reactions.

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Hyperthermia Protects Against Light Damage in the Rat Retina

Cited by 402 publications

References 20 publications

Induced Tolerance to Ischemia in Gerbil Hippocampal Neurons

Induced Tolerance to Ischemia in Gerbil Hippocampal Neurons

Hsp70 Inhibits Aminoglycoside-Induced Hair Cell Death and is Necessary for the Protective Effect of Heat Shock

A note on heat shock protein 70 expression in goats subjected to road transportation under hot, humid tropical conditions

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