Characterization of the Larynx in Ephrin-B2 Knockout Mice: A Novel Animal Model for Laryngeal Clefts | Congenital Defects | JAMA Otolaryngology–Head & Neck Surgery | JAMA Network
[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 34.234.207.100. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Original Article
Oct 2012

Characterization of the Larynx in Ephrin-B2 Knockout Mice: A Novel Animal Model for Laryngeal Clefts

Author Affiliations

Author Affiliations: Departments of Otolaryngology–Head and Neck Surgery (Drs Neilan, Shao, and Lee) and Developmental Biology (Drs Dravis and Henkemeyer), University of Texas Southwestern Medical Center, Dallas.

Arch Otolaryngol Head Neck Surg. 2012;138(10):969-972. doi:10.1001/archotol.2013.109
Abstract

Objective To identify and classify laryngeal clefts in a novel mouse model.

Design In vivo animal study.

Setting Academic research laboratory.

Subjects 129/CD1 mice with the ephrin-B2 gene disrupted by the β-galactosidase (lacZ) gene were humanely killed at embryonic day 18 (E18) and evaluated for the presence and characterization of a laryngeal cleft. Homozygous and heterozygous lacZ knockout mice as well as wild-type littermates were evaluated.

Main Outcome Measures Microsurgical dissection of the oral cavity and pharynx allowed for a pseudoendoscopic view of the larynx to determine the presence or absence of a cleft. The specimens were also histologically sectioned and examined for characterization and classification of the cleft.

Results A laryngeal cleft was identified in 12 of 27 ephrin-B2 homozygous lacZ knockout mice (44%). Laryngeal clefts were not identified in heterozygous ephrin-B2 knockout mice or in wild-type littermates.

Conclusions Disruption of ephrin-B2 reverse signaling results in laryngeal clefts in lacZ knockout mice. This presents a novel mouse model in which future investigations into etiology of laryngeal clefts may be examined.

×