Comparison of Ephrin-A ligand and EphA receptor distribution in the developing inner ear

Title:
Comparison of Ephrin-A ligand and EphA receptor distribution in the developing inner ear
Authors:
Bianchi, Lynne M.; Liu, H.
Abstract:
Members of the recently discovered Eph family appear to play important roles in a variety of developmental processes including tissue segmentation, cell migration and axonal guidance. To begin to understand the functions of the EphA subclass of receptors and their corresponding GPI-linked (ephrin-A) ligands in the inner ear, a developmental immunohistochemical analysis was completed. The results indicated that the ligands ephrin-A1 and ephrin-A2 were localized mainly at cellular boundaries in the inner ear. Ephrin-A1 was detected mainly in the epithelial cells lining the fluid filled ducts of the inner ear, whereas ephrin-A2 was prominently expressed in connective tissue regions. The receptor EphA4 was detected in vestibular hair cells. EphA5 and EphA7 were detected mainly in cochlear and vestibular supporting cells. These results suggest that these Eph molecules play a role in establishing the formation and cellular organization of the complex inner ear labyrinth. Additionally, all of the ligands and receptors evaluated were expressed in vestibular and cochlear neurons at various developmental stages, suggesting they may play a role in establishing or maintaining innervation to the inner ear.
Citation:
Bianchi, L.M., and H. Liu. 1999. "Comparison of Ephrin-A ligand and EphA receptor distribution in the developing inner ear." The Anatomical Record 254(1): 127-134.
Publisher:
John Wiley & Sons
DATE ISSUED:
1999-01-01
Department:
Neuroscience
Type:
article
PUBLISHED VERSION:
10.1002/(SICI)1097-0185(19990101)254:1<127
PERMANENT LINK:
http://hdl.handle.net/11282/309728

Full metadata record

DC FieldValue Language
dc.contributor.authorBianchi, Lynne M.en_US
dc.contributor.authorLiu, H.en_US
dc.date.accessioned2013-12-23T16:16:27Zen
dc.date.available2013-12-23T16:16:27Zen
dc.date.issued1999-01-01en
dc.identifier.citationBianchi, L.M., and H. Liu. 1999. "Comparison of Ephrin-A ligand and EphA receptor distribution in the developing inner ear." The Anatomical Record 254(1): 127-134.en_US
dc.identifier.issn0003-276Xen_US
dc.identifier.urihttp://hdl.handle.net/11282/309728en
dc.description.abstractMembers of the recently discovered Eph family appear to play important roles in a variety of developmental processes including tissue segmentation, cell migration and axonal guidance. To begin to understand the functions of the EphA subclass of receptors and their corresponding GPI-linked (ephrin-A) ligands in the inner ear, a developmental immunohistochemical analysis was completed. The results indicated that the ligands ephrin-A1 and ephrin-A2 were localized mainly at cellular boundaries in the inner ear. Ephrin-A1 was detected mainly in the epithelial cells lining the fluid filled ducts of the inner ear, whereas ephrin-A2 was prominently expressed in connective tissue regions. The receptor EphA4 was detected in vestibular hair cells. EphA5 and EphA7 were detected mainly in cochlear and vestibular supporting cells. These results suggest that these Eph molecules play a role in establishing the formation and cellular organization of the complex inner ear labyrinth. Additionally, all of the ligands and receptors evaluated were expressed in vestibular and cochlear neurons at various developmental stages, suggesting they may play a role in establishing or maintaining innervation to the inner ear.en_US
dc.language.isoen_USen_US
dc.publisherJohn Wiley & Sonsen_US
dc.identifier.doi10.1002/(SICI)1097-0185(19990101)254:1<127en
dc.subject.departmentNeuroscienceen_US
dc.titleComparison of Ephrin-A ligand and EphA receptor distribution in the developing inner earen_US
dc.typearticleen_US
dc.identifier.journalAnatomical Recorden_US
dc.subject.keywordEphen_US
dc.subject.keywordImmunohistochemistryen_US
dc.subject.keywordHair cellen_US
dc.subject.keywordGerbilen_US
dc.subject.keywordAuditoryen_US
dc.identifier.volume254en_US
dc.identifier.issue1en_US
dc.identifier.startpage127en_US
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