The Coxsackievirus and Adenovirus Receptor: A new adhesion protein in cochlear development

Excoffon, Katherine J. D. A.; Avenarius, Matthew R.; Hansen, Marlan R.; Kimberling, William J.; Najmabadi, Hossein; Smith, Richard J.H.; Zabner, Joseph

doi:10.1016/j.heares.2006.02.009

Cited by 26 publications

(17 citation statements)

References 37 publications

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“…Most other groups have found that hair cells are not typically transduced in mice when adenovirus is applied to scala tympani (13,14,17). This is consistent with the recent report that hair cells in the mouse cochlea lose their coxsackie-adenovirus receptors before adulthood (41). However, it should be noted that 2 groups have demonstrated mouse hair cell infection using adenoviral vectors with a scala tympani inoculation technique (13,20,42).…”

Section: Discussionsupporting

confidence: 75%

Helper-Dependent Adenovirus-Mediated Gene Transfer Into the Adult Mouse Cochlea

Wenzel¹,

Xia²,

Funk³

et al. 2007

Otology &Amp; Neurotology

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Section: Discussionsupporting

confidence: 75%

Helper-Dependent Adenovirus-Mediated Gene Transfer Into the Adult Mouse Cochlea

Wenzel¹,

Xia²,

Funk³

et al. 2007

Otology &Amp; Neurotology

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“…CAR is present in cells of the auditory epithelium but its distribution does not completely explain the pattern of cellular transduction in this epithelium, during development and in the mature tissue [28, 29]. Lack of transgene expression in hair cells is especially intriguing, considering the presence of CAR in these cells.…”

Section: Characteristics Of Adenoviral Gene Transduction In the Innermentioning

confidence: 99%

Gene Therapy in the Inner Ear Using Adenovirus Vectors

Husseman

Raphael

2009

Gene Therapy of Cochlear Deafness

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Therapies for the protection and regeneration of auditory hair cells are of great interest given the significant monetary and lifestyle impact of hearing loss. The past decade has seen tremendous advances in the use of adenoviral vectors to achieve these aims. Preliminary data demonstrated the functional capacity of this technique as adenoviral-induced expression of neurotrophic and growth factors protected hair cells and spiral ganglion neurons from ototoxic insults. Subsequent efforts confirmed the feasibility of adenoviral transfection of cells in the auditory neuroepithelium via cochleostomy into the scala media. Most recently, efforts have focused on regeneration of depleted hair cells. Mammalian hearing loss is generally considered a permanent insult as the auditory epithelium lacks a basal layer capable of producing new hair cells. Recently, the transcription factor Atoh1 has been found to play a critical role in hair cell differentiation. Adenoviral-mediated overexpression of Atoh1 in culture and in vivo have shown the ability to regenerate auditory and vestibular hair cells by causing transdifferentiation of neighboring epithelial-supporting cells. Functional recovery of both the auditory and vestibular systems has been documented following adenoviral induced Atoh1 overexpression.

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“…14 Adenoviral receptors are expressed in a wide range of cell subtypes and gene delivery is a function of the expression level of these receptors. [15][16][17] Only one study concerns the expression and the localization of adenoviral receptors in the mammalian cochlea, 18 and no data have been reported after application of adenovirus in the rat cochlea in vivo.…”

Section: Introductionmentioning

confidence: 99%

Coxsackie adenovirus receptor and ανβ3/ανβ5 integrins in adenovirus gene transfer of rat cochlea

et al. 2006

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This study was designed to determine whether Coxsackie adenovirus receptor (CAR) and anb3/anb5 integrin co-receptors are involved in adenovirus gene transfer in the rat cochlea. We find that CAR and integrin co-receptors are expressed in every cell subtype transduced by the adenoviral vector Ad5 DE1-E3/cytomegalovirus/green fluorescent protein (GFP) on cochlear slices in vitro. The spiral ganglion neurons, which do not express CAR, were not transduced by the virus. Blocking these receptors by monoclonal antibodies decreased transgene expression, whereas disrupting tight junctions with ethylenediaminetetraacetic acid led to an increased transgene expression. However, sensory hair cells and strial cells also expressing CAR and an integrins were not transduced by the vector.GFP expression was also studied in vivo. Perilymphatic perfusion of adenovirus in vivo did not affect hearing and only cells lining the perilymphatic spaces were transduced. Endolymphatic perfusion resulted in low-frequency hearing loss and although some cells of the organ of Corti were efficiently transduced, the sensory and the strial cells were not. Transduced sensory and strial cells were occasionally observed in cochleas after single shot of adenovirus. Pretreatment with anti-CAR and anti-an antibodies decreases GFP expression in vivo, suggesting that the CAR/an integrin pathway is involved in adenovirus transduction in the cochlea.

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The Coxsackievirus and Adenovirus Receptor: A new adhesion protein in cochlear development

Cited by 26 publications

References 37 publications

Helper-Dependent Adenovirus-Mediated Gene Transfer Into the Adult Mouse Cochlea

Helper-Dependent Adenovirus-Mediated Gene Transfer Into the Adult Mouse Cochlea

Gene Therapy in the Inner Ear Using Adenovirus Vectors

Coxsackie adenovirus receptor and ανβ3/ανβ5 integrins in adenovirus gene transfer of rat cochlea

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