Functional auditory hair cells produced in the mammalian cochlea by in utero gene transfer

Samuel P. Gubbels, David W. Woessner, John C. Mitchell, Anthony J. Ricci and John V. Brigande ()
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Samuel P. Gubbels: Oregon Hearing Research Center, and
David W. Woessner: Oregon Hearing Research Center, and
John C. Mitchell: School of Dentistry, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA
Anthony J. Ricci: Stanford University School of Medicine, 801 Welch Road, Stanford, California 94305, USA
John V. Brigande: Oregon Hearing Research Center, and

Nature, 2008, vol. 455, issue 7212, 537-541

Abstract: Hair-cell triggers Cochlear hair cells form the sound-sensing apparatus of vertebrates and their loss or damage results in hearing impairment. Mammals cannot regenerate these cells, but previous work has shown that ectopic expression of the transcription factor Atonal homologue 1 (Atoh1) can induce cells that would not normally differentiate as cochlear hair cells to become hair cell-like. Now Gubbels et al. show that in utero gene transfer of Atoh1 into mouse cochleas generates ectopic hair cells in the cochlea. Importantly, these supernumerary hair cells are functionally competent and display neuronal connectivity. This is a major step towards experiments to test for the ability of gene therapies to ameliorate hearing loss in mouse models of human deafness.

Date: 2008
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DOI: 10.1038/nature07265

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