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Titolo:
Calpain inhibitors protect auditory sensory cells from hypoxia and neurotrophin-withdrawal induced apoptosis
Autore:
Cheng, AG; Huang, T; Stracher, A; Kim, A; Liu, W; Malgrange, B; Lefebvre, PP; Schulman, A; Van de Water, TR;
Indirizzi:
Albert Einstein Coll Med, Dept Otolaryngol, Rose F Kennedy Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 nedy Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10467 USA Albert Einstein Coll Med Bronx NY USA 10467 Neurosci, Bronx, NY 10467 USA SUNY Hlth Sci Ctr, Dept Biochem, Brooklyn, NY 11203 USA SUNY Hlth Sci CtrBrooklyn NY USA 11203 t Biochem, Brooklyn, NY 11203 USA SUNY Hlth Sci Ctr, Clin Otolaryngol, Brooklyn, NY 11203 USA SUNY Hlth Sci Ctr Brooklyn NY USA 11203 olaryngol, Brooklyn, NY 11203 USA Univ Liege, Dept Human Physiol & Pathophysiol, Liege, Belgium Univ Liege Liege Belgium t Human Physiol & Pathophysiol, Liege, Belgium
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 850, anno: 1999,
pagine: 234 - 243
SICI:
0006-8993(199912)850:1-2<234:CIPASC>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
PRODUCT OTOACOUSTIC EMISSIONS; CIS-DIAMMINEDICHLOROPLATINUM; CISPLATIN OTOTOXICITY; CASPASE INHIBITORS; CEREBRAL-ISCHEMIA; GANGLION NEURONS; OXIDATIVE STRESS; ACOUSTIC TRAUMA; HEARING-LOSS; GUINEA-PIG;
Keywords:
apoptosis; auditory system; calpain; neurotrophin-withdrawal; hypoxia; noise trauma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Van de Water, TR Albert Einstein Coll Med, Dept Otolaryngol, Rose F Kennedy Ctr, Room 302,1410 Pelham Pkwy S, Bronx, NY 10461 USA Albert Einstein Coll Med Room 302,1410 Pelham Pkwy S Bronx NY USA 10461
Citazione:
A.G. Cheng et al., "Calpain inhibitors protect auditory sensory cells from hypoxia and neurotrophin-withdrawal induced apoptosis", BRAIN RES, 850(1-2), 1999, pp. 234-243

Abstract

Inhibitors of calpain have been shown to protect nerve growth factor (NGF)-deprived ciliary ganglion neurons and hypoxic cortical neurons. Calpains have been identified in the cochlea and are active during ischemic injury. Since apoptosis can be initiated by loss of neurotrophic support, hypoxia, and ototoxins (e.g., cisplatin, CDDP), the role of calpain inhibitors under these conditions was examined in auditory hair cells and neurons. Dissociated spiral ganglion neuron(SGN) cell cultures and organ of Corti explants from P3 rats were used to test the efficacy of calpain inhibitors as otoprotective molecules. Our results indicate that calpain inhibitor I, calpain inhibitor II, and leupeptin all provided significant protection of SGNs against neurotrophin-withdrawal and hypoxia-induced apoptosis. The increase in neuronal survival ranged from 2.16 to 2.31 times greater than in untreated neurotrophin-withdrawn SGN cell cultures. BOC-Asp(Ome)-Fluoromethyl Ketone (B-D-FMK), a general caspase inhibitor, increased neuronal survival 2.16 times more. Neuronal survival rates were from 1.88 to 2.27 times greater than in untreated, hypoxic neurons and hair cell survival rates were from 1.98 to2.03 times greater than untreated, hypoxic organ of Corti explants. However, protection of auditory hair cells and neurons from CDDP-induced damage (10 and 6 mu g/ml, respectively) was limited with any of these calpain inhibitors. Apoptotic pathways initiated by neurotropbin-deprivation and ototoxic stress (e.g., CDDP) have been shown to be different,Our results agree with this finding, with neurotrophin-withdrawal and hypoxia, but not CDDP damage-induced apoptosis being calpain-dependent. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 16/07/20 alle ore 15:38:04