Linked Life Data

11850449

Source:http://linkedlifedata.com/resource/pubmed/id/11850449

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-2-18
pubmed:abstractText
Sensory hair cells die after acoustic trauma or ototoxic insults, but the signal transduction pathways that mediate hair cell death are not known. Here we identify several important signaling events that regulate the death of vestibular hair cells. Chick utricles were cultured in media supplemented with the ototoxic antibiotic neomycin and selected pharmacological agents that influence signaling molecules in cell death pathways. Hair cells that were treated with neomycin exhibited classically defined apoptotic morphologies such as condensed nuclei and fragmented DNA. Inhibition of protein synthesis (via treatment with cycloheximide) increased hair cell survival after treatment with neomycin, suggesting that hair cell death requires de novo protein synthesis. Finally, the inhibition of caspases promoted hair cell survival after neomycin treatment. Sensory hair cells in avian vestibular organs also undergo continual cell death and replacement throughout mature life. It is unclear whether the loss of hair cells stimulates the proliferation of supporting cells or whether the production of new cells triggers the death of hair cells. We examined the effects of caspase inhibition on spontaneous hair cell death in the chick utricle. Caspase inhibitors reduced the amount of ongoing hair cell death and ongoing supporting cell proliferation in a dose-dependent manner. In isolated sensory epithelia, however, caspase inhibitors did not affect supporting cell proliferation directly. Our data indicate that ongoing hair cell death stimulates supporting cell proliferation in the mature utricle.
pubmed:grant
pubmed:keyword
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1218-27
pubmed:dateRevised
2011-8-1
pubmed:meshHeading
pubmed-meshheading:11850449-Amino Acid Chloromethyl Ketones, pubmed-meshheading:11850449-Animals, pubmed-meshheading:11850449-Anti-Bacterial Agents, pubmed-meshheading:11850449-Apoptosis, pubmed-meshheading:11850449-Calcium-Binding Protein, Vitamin D-Dependent, pubmed-meshheading:11850449-Caspases, pubmed-meshheading:11850449-Cell Count, pubmed-meshheading:11850449-Cell Division, pubmed-meshheading:11850449-Cell Nucleus, pubmed-meshheading:11850449-Cell Survival, pubmed-meshheading:11850449-Chickens, pubmed-meshheading:11850449-Chromatin, pubmed-meshheading:11850449-Enzyme Inhibitors, pubmed-meshheading:11850449-Hair Cells, Auditory, pubmed-meshheading:11850449-Neomycin, pubmed-meshheading:11850449-Organ Culture Techniques, pubmed-meshheading:11850449-Protein Synthesis Inhibitors, pubmed-meshheading:11850449-Saccule and Utricle
pubmed:year
2002
pubmed:articleTitle
Inhibition of caspases prevents ototoxic and ongoing hair cell death.
pubmed:affiliation
Central Institute for the Deaf, Fay and Carl Simons Center for Biology of Hearing and Deafness, Washington University School of Medicine, St. Louis, Missouri 63110, USA. jmatsui@cid.wustl.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't