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Home | Pregnancy Timeline | News Alerts |News Archive Nov 20, 2014

Microscopic view of cells deep within the ear of a newborn mouse. Shown in red
and blue, the supporting cells surround the green hair cells that send sound.




A potential way to restore hearing

Harnessing the regenerative power of early support cells could lead to new strategies to combat many causes of deafness.

There are many kinds of tiny cells working together that give us the ability to hear. "Hair cells" are crucial in carrying sound signals to the brain. But new research shows that the ear's support cells are key to preserving hearing. And when it comes to restoring lost hearing, support cells may be regenerable.

In work published online in the Proceedings of the National Academy of Sciences, researchers from the University of Michigan (U-M) Medical School, and colleagues from St. Jude Children's Research Hospital report findings from in-depth studies of these support cells.

The research reveals that damage to support cells in the mature mouse results in the loss of hair cells which leads to profound deafness.

But the big surprise is that in the newborn mouse, the ear rapidly regenerates new support cells - resulting in complete preservation of hearing. Regeneration is the outcome of adjacent cells moving into proximity and taking on the role of full-fledged support cells.

The finding not only shows that deafness can result from loss of support cells — it reveals a previously unknown ability of mice to regenerate support cells only a few days following birth. If scientists can determine what's going on inside those newly formed support cells, they might be able to harness and command new approaches to regenerating auditory cells to restore hearing in humans.

Senior author and U-M Kresge Hearing Research Institute director Gabriel Corfas, Ph.D., says his research shows that support cells play a more critical role in hearing than previously understood.

Corfas: "We had known that losing hair cells results in deafness, and there has been an effort to find a way to regenerated these specialized cells. One idea has been to induce support cells to become hair cells. Now we discover that losing support cells kills hair cells as well."

"And now, we've found that there's an intrinsic regenerative potential in the very early days of life that we could harness as we work to cure deafness. This is relevant to many forms of inherited and congenital deafness, and hearing loss due to age and noise exposure. If we can identify the molecules that are responsible for this regeneration, we may be able to turn back the clock inside these ears and regenerate lost cells."

In the research, support cells found in a structure called the greater epithelial ridge transformed into full-fledged support cells after the researchers destroyed the mice's own with a precisely targeted toxin that didn't affect hair cells. The new cells differentiated into those that had been lost, called inner border cells and inner phalangeal cells.

"Hair cell loss can be a consequence of support cell dysfunction or loss, suggesting that in many cases deafness could be primarily a support cell disease. Understanding the mechanisms that underlie these processes should help in the development of regenerative medicine strategies to treat deafness and vestibular disorders."

Gabriel Corfas PhD, senior author, professor Department of Otolaryngology, University of Michigan Medical School, and Kresge Hearing Research Institute director

Making sure that the inner ear has enough support cells, which themselves can transform into hair cells, will be a critical upstream step for any regenerative approach. Corfas and colleagues continue to work, hoping to find drugs that can trigger the same regenerative powers they found in newborn mice.


The auditory sensory epithelium contains two major cell types: hair cells and supporting cells. Mammalian auditory hair cells do not regenerate after damage or loss, resulting in permanent hearing impairment. How supporting cell loss affects auditory function remains to be determined. Here, we demonstrate that inner border and inner phalangeal cells, the two types of supporting cells surrounding inner hair cells, can be replenished completely after selective ablation in the neonatal cochlea, allowing hearing to be preserved. Our findings challenge the view that mammalian auditory sensory epithelium has limited intrinsic regenerative capacity and provide previously unindetified opportunities for replacement of damaged auditory cells and restoration of hearing.

Supporting cells in the cochlea play critical roles in the development, maintenance, and function of sensory hair cells and auditory neurons. Although the loss of hair cells or auditory neurons results in sensorineural hearing loss, the consequence of supporting cell loss on auditory function is largely unknown. In this study, we specifically ablated inner border cells (IBCs) and inner phalangeal cells (IPhCs), the two types of supporting cells surrounding inner hair cells (IHCs) in mice in vivo. We demonstrate that the organ of Corti has the intrinsic capacity to replenish IBCs/IPhCs effectively during early postnatal development. Repopulation depends on the presence of hair cells and cells within the greater epithelial ridge and is independent of cell proliferation. This plastic response in the neonatal cochlea preserves neuronal survival, afferent innervation, and hearing sensitivity in adult mice. In contrast, the capacity for IBC/IPhC regeneration is lost in the mature organ of Corti, and consequently IHC survival and hearing sensitivity are impaired significantly, demonstrating that there is a critical period for the regeneration of cochlear supporting cells. Our findings indicate that the quiescent neonatal organ of Corti can replenish specific supporting cells completely after loss in vivo to guarantee mature hearing function.

The research was a partnership between Corfas' team at U-M and that of Jian Zuo, Ph.D., of St. Jude, and the two share senior authorship. Marcia M. Mellado Lagarde, Ph.D. of St. Jude and Guoqiang Wan, Ph.D., of U-M are co-first authors. Additional authors are LingLi Zhang of St. Jude, Corfas' former colleagues at Harvard University Angelica R. Gigliello and John J. McInnis; and Yingxin Zhang and Dwight Bergles, both of Johns Hopkins University.

Reference: PNAS 2014 ; published ahead of print, doi:10.1073/pnas.1408064111

The research was funded by a Sir Henry Wellcome Fellowship, a Hearing Health Foundation Emerging Research Grant, the Boston Children's Hospital Otolaryngology Foundation, National Institutes of Health grants DC004820, HD18655, DC006471, and CA21765; Office of Naval Research Grants N000140911014, N000141210191, and N000141210775, and by the American Lebanese Syrian Associated Charities of St. Jude Children's Research Hospital.


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