Expression of heat shock protein, HSP72, in the guinea pig and rat cochlea after hyperthermia: Immunochemical and in situ hybridization analysis

Dechesne, Claude J.; Kim, Hong N.; Nowak, Thaddeus S.; Wenthold, Robert J.

doi:10.1016/0378-5955(92)90116-5

Cited by 48 publications

(33 citation statements)

References 30 publications

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“…In order to begin to develop Hsp70 as an otoprotective therapy against aminoglycoside-induced hearing loss, a safe method of Hsp70 induction is required. Total body heat shock induces Hsp70 in guinea pig and mouse cochleae (Dechesne et al 1992;Yoshida et al 1999;Sugahara et al 2003). In addition, local heat shock can induce Hsp70 in the inner ear (Sugahara et al 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Thus it seems unlikely that systemic caspase inhibitors or JNK inhibitors will be developed into safe and viable cotherapies aimed at inhibiting aminoglycoside-induced ototoxicity. However, it is possible to safely induce Hsp70 in the whole organism, either by experimental manipulation (heat stress) (Dechesne et al 1992;Yoshida et al 1999;Sugahara et al 2003) or by administration of a therapeutic agent (Hirakawa et al 1996;Ooie et al 2001;Oda et al 2002;Mikuriya et al 2005;Sone et al 2005). In order to begin to develop Hsp70 as an otoprotective therapy against aminoglycoside-induced hearing loss, a safe method of Hsp70 induction is required.…”

Section: Discussionmentioning

confidence: 99%

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Hsp70 inhibits aminoglycoside-induced hearing loss and cochlear hair cell death

Taleb

Brandon

Lee

et al. 2009

Cell Stress and Chaperones

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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 c-Jun N-terminal kinase (JNK) and caspases. Induction of heat shock proteins (Hsps) can inhibit JNK-and caspase-dependent apoptosis in a variety of systems. We have previously shown that heat shock results in 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 this system, Hsp70 is the most strongly induced Hsp, which is upregulated over 250-fold at the level of mRNA 2 h after heat shock. Hsp70 overexpression inhibits aminoglycoside-induced hair cell death in vitro. In this study, we utilized Hsp70-overexpressing mice to determine whether Hsp70 is protective in vivo. Both Hsp70-overexpressing mice and their wildtype littermates were treated with systemic kanamycin (700 mg/kg body weight) twice daily for 14 days. While kanamycin treatment resulted in significant hearing loss and hair cell death in wild-type mice, Hsp70-overexpressing mice were significantly protected against aminoglycosideinduced hearing loss and hair cell death. These data indicate that Hsp70 is protective against aminoglycoside-induced ototoxicity in vivo.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Hsp70 inhibits aminoglycoside-induced hearing loss and cochlear hair cell death

Taleb

Brandon

Lee

et al. 2009

Cell Stress and Chaperones

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“…53 We showed that mRNA granules correlated with long-term TA but that colocalization of ELAV proteins with mRNA granules correlated with the survival of CA3 neurons and translation of the stress protein HSP70, 13 suggesting a defect in postischemic mRNA regulation. A defect in mRNA regulation is also consistent with lack of translation of HSP70 protein in CA1 in spite of its copious transcription, 33,[54][55][56][57][58][59] which was also observed for stress mRNAs induced by the unfolded protein response. [60][61][62] Differences in mRNA handling by CA1 and CA3 are supported by our observation that HuB, HuC, and HuD are absent in CA1, but not CA3, control neurons.…”

Section: Mrna Dysfunction After Brain I/rmentioning

confidence: 84%

Embryonic lethal abnormal vision proteins and adenine and uridine-rich element mRNAs after global cerebral ischemia and reperfusion in the rat

Wang

Anggraini

DeGracia

2016

J Cereb Blood Flow Metab

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Prolonged translation arrest correlates with delayed neuronal death of hippocampal CA1 neurons following global cerebral ischemia and reperfusion. Many previous studies investigated ribosome molecular biology, but mRNA regulatory mechanisms after brain ischemia have been less studied. Here we investigated the embryonic lethal abnormal vision/Hu isoforms HuR, HuB, HuC, and HuD, as well as expression of mRNAs containing adenine and rich uridine elements following global ischemia in rat brain. Proteomics of embryonic lethal abnormal vision immunoprecipitations or polysomes isolated from rat hippocampal CA1 and CA3 from controls or following 10 min ischemia plus 8 h of reperfusion showed distinct sets of mRNA-binding proteins, suggesting differential mRNA regulation in each condition. Notably, HuB, HuC, and HuD were undetectable in NIC CA1. At 8 h reperfusion, polysome-associated mRNAs contained 46.1% of ischemia-upregulated mRNAs containing adenine and rich uridine elements in CA3, but only 18.7% in CA1. Since mRNAs containing adenine and rich uridine elements regulation are important to several cellular stress responses, our results suggest CA1 is disadvantaged compared to CA3 in coping with ischemic stress, and this is expected to be an important contributing factor to CA1 selective vulnerability. (Data are available via ProteomeXchange identifier PXD004078 and GEO Series accession number GSE82146).Keywords Global brain ischemia and reperfusion, hippocampal CA1, adenine and rich uridine elements mRNA, embryonic lethal abnormal vision, mRNA regulation

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“…While the normal, non-stressed guinea pig cochlea has a high level of expression of HSP 72 in many regions (Neely et al, 1991), a heat induced increased expression of HSP 72 immunoreactivity in interdental cells of the spiral limbus was observed by Thompson et al (1992). Dechesne et al, (1992) and Myers et al (1992) found no HSP 72 expression in the normal, non-stressed, rat cochleae and induced expression using heat and hypoxia respectively. We stimulated rats with intense noise, a stress that is more specific and common to the cochlea.…”

Section: Discussionmentioning

confidence: 99%

“…HSPs are believed to be induced by moderate stresses in order to protect the cells from even more severe stresses (Lindquist and Craig, 1988) and it can be hypothesized that HSPs may have some responsibilities in protective mechanism of hair cells against various kinds of insults. In the peripheral auditory system several investigators have demonstrated the induction of HSP 72 with hyperthermia in the rat cochlea (Dechesne et al, 1992) and guinea pig cochlea (Thompson et al, 19921, as well as with transient ischemia in the rat cochlea (Myers et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Detection of HSP 72 synthesis after acoustic overstimulation in rat cochlea

et al. 1993

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The purpose of this study was to determine if high intensity acoustic stimulation would induce HSP 72 in rat cochlea. The animals were exposed to 110 dB SPL broad band noise for 1.5 h and sacrificed 4, 6 and 8 h after stimulation.Immunocytochemistry and western blotting were used to detect the expression of HSP 72 in the cochlear tissues. Western blots showed an intense 72 kD band in the noise exposed animals compared to a very light band in non-stimulated control animals. Immunocytochemical results in the cochlea revealed noise induced HSP 72 immunoreactive staining of outer hair cells. Only a few immunoreactive stained inner hair cells were seen and spiral ganglion cells were not stained. These results indicate that acoustic overstimulation can induce the expression of HSP 72 in outer hair cells of the rat cochlea. HSP 72 may serve as a marker for cellular stress and potential damage and may be involved in protection from insult.

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Expression of heat shock protein, HSP72, in the guinea pig and rat cochlea after hyperthermia: Immunochemical and in situ hybridization analysis

Cited by 48 publications

References 30 publications

Hsp70 inhibits aminoglycoside-induced hearing loss and cochlear hair cell death

Hsp70 inhibits aminoglycoside-induced hearing loss and cochlear hair cell death

Embryonic lethal abnormal vision proteins and adenine and uridine-rich element mRNAs after global cerebral ischemia and reperfusion in the rat

Detection of HSP 72 synthesis after acoustic overstimulation in rat cochlea

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