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Kanamycin alters cytoplasmic and nuclear phosphoinositide signaling in the organ of Corti in vivo

dc.contributor.authorJiang, Hongyanen_US
dc.contributor.authorSha, Su-Huaen_US
dc.contributor.authorSchacht, Jochenen_US
dc.date.accessioned2010-04-01T14:43:21Z
dc.date.available2010-04-01T14:43:21Z
dc.date.issued2006-10en_US
dc.identifier.citationJiang, Hongyan; Sha, Su-Hua; Schacht, Jochen (2006). "Kanamycin alters cytoplasmic and nuclear phosphoinositide signaling in the organ of Corti in vivo ." Journal of Neurochemistry 99(1): 269-276. <http://hdl.handle.net/2027.42/65167>en_US
dc.identifier.issn0022-3042en_US
dc.identifier.issn1471-4159en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/65167
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=16903869&dopt=citationen_US
dc.description.abstractAminoglycoside antibiotics strongly bind to phosphoinositides and affect their membrane distribution and metabolism. Kanamycin treatment also disrupts Rac/Rho signaling pathways to the actin cytoskeleton in the mouse inner ear in vivo . Here, we investigate the influence of kanamycin on phosphoinositide signaling in sensory cells (hair cells) of the mouse cochlea. Immunoreactivity to phosphatidylinositol-3,4,5-trisphosphate (PIP 3 ) decreased in the organ of Corti, especially in outer hair cells, after 3–7 days of drug treatment, whereas imunoreactivity to phosphatidylinositol-4,5-bisphosphate (PIP 2 ) increased. Immunoreactivity to PIP 2 was present at the apical poles of outer hair cells, but appeared in their nuclei only after drug treatment. Furthermore, nuclear PIP 2 formed a complex with histone H3 and attenuated its acetylation in outer hair cells. In agreement with reduced PIP 3 signaling, phosphorylated Akt decreased in both the cytoplasm and nuclei of outer hair cells after kanamycin treatment. This study suggests that kanamycin disturbs the balance between PIP 2 and PIP 3 , modifies gene transcription via histone acetylation and diminishes the PI3K/Akt survival pathway. These actions may contribute to the death of outer hair cells, which is a consequence of chronic kanamycin treatment.en_US
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dc.format.extent3110 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Publishing Ltden_US
dc.rights2006 The Authors Journal Compilation 2006 International Society for Neurochemistryen_US
dc.subject.otherAkten_US
dc.subject.otherHistoneen_US
dc.subject.otherOuter Hair Cellsen_US
dc.subject.otherPhosphatidylinositol-4, 5-bisphosphateen_US
dc.subject.otherPhosphatidylinositol-3, 4, 5-trisphosphateen_US
dc.subject.otherSignaling Pathwaysen_US
dc.titleKanamycin alters cytoplasmic and nuclear phosphoinositide signaling in the organ of Corti in vivoen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationum* Kresge Hearing Research Institute, Department of Otolaryngology, University of Michigan, Ann Arbor, Michigan, USAen_US
dc.contributor.affiliationother† Otorhinolaryngological Hospital of First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Chinaen_US
dc.identifier.pmid16903869en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/65167/1/j.1471-4159.2006.04117.x.pdf
dc.identifier.doi10.1111/j.1471-4159.2006.04117.xen_US
dc.identifier.sourceJournal of Neurochemistryen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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