Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-8-15
pubmed:abstractText
Exposure to loud noise can induce temporary or permanent hearing loss, and acoustic trauma is the major cause of hearing impairment in industrial nations. However, the mechanisms underlying the death of hair cells after acoustic trauma remain unclear. In addition to its involvement in cellular stress and apoptosis, the c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family, is involved in cell survival, transformation, embryonic morphogenesis, and differentiation. JNK is primarily activated by various environmental stresses including noise, and the phenotypic result appears be to cell death. All-trans retinoic acid (ATRA) is an active metabolite of vitamin A that regulates a wide range of biological processes, including cell proliferation, differentiation, and morphogenesis. We evaluated the role of ATRA in preserving hearing in mice exposed to noise that can induce permanent hearing loss. Mice fed with ATRA before and during 3 consecutive days of noise exposure had a more preserved hearing threshold than mice fed sesame oil or saline. Histological and TUNEL staining of the cochlea showed significantly enhanced preservation of the organ of Corti, including outer hair cells and relatively low apoptotic nuclei, in mice-fed ATRA than in mice-fed sesame oil or saline. Phospho-JNK immunohistochemistry showed that ATRA inhibited the activation of JNK. These results suggest that ATRA has an anti-apoptotic effect on cochleae exposed to noise.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
335
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
485-90
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16084493-Animals, pubmed-meshheading:16084493-Apoptosis, pubmed-meshheading:16084493-Cell Differentiation, pubmed-meshheading:16084493-Cell Proliferation, pubmed-meshheading:16084493-Cell Survival, pubmed-meshheading:16084493-Cochlea, pubmed-meshheading:16084493-Ear, Inner, pubmed-meshheading:16084493-Epithelium, pubmed-meshheading:16084493-Hair Cells, Auditory, pubmed-meshheading:16084493-Hearing Loss, pubmed-meshheading:16084493-Hearing Loss, Noise-Induced, pubmed-meshheading:16084493-Immunohistochemistry, pubmed-meshheading:16084493-In Situ Nick-End Labeling, pubmed-meshheading:16084493-JNK Mitogen-Activated Protein Kinases, pubmed-meshheading:16084493-MAP Kinase Kinase 4, pubmed-meshheading:16084493-MAP Kinase Signaling System, pubmed-meshheading:16084493-Mice, pubmed-meshheading:16084493-Mice, Inbred BALB C, pubmed-meshheading:16084493-Mitogen-Activated Protein Kinase Kinases, pubmed-meshheading:16084493-Noise, pubmed-meshheading:16084493-Organ of Corti, pubmed-meshheading:16084493-Time Factors, pubmed-meshheading:16084493-Tretinoin
pubmed:year
2005
pubmed:articleTitle
Anti-apoptotic role of retinoic acid in the inner ear of noise-exposed mice.
pubmed:affiliation
Department of Otolaryngology, Asan Medical Center, University of Ulsan, College of Medicine, Seoul, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't