We've updated our Privacy Policy to make it clearer how we use your personal data.

We use cookies to provide you with a better experience. You can read our Cookie Policy here.

Advertisement

Discovered Process Allows Damaged Hair Cells To Repair Themselves

A human ear on a white background.
Credit: Franco Antonio Giovanella / Unsplash.
Listen with
Speechify
0:00
Register for free to listen to this article
Thank you. Listen to this article using the player above.

Want to listen to this article for FREE?

Complete the form below to unlock access to ALL audio articles.

Read time: 3 minutes

Summary

UVA researchers reveal the remarkable resilience of inner ear hair cells, capable of self-repair from loud noise and stress. XIRP2 protein orchestrates the restoration of damaged core structures, inspiring hopes for improved hearing loss treatments and potential insights into Alzheimer's and related conditions.

Key takeaways

  • Researchers at UVA School of Medicine have discovered that hair cells in the inner ear, responsible for hearing and balance, have the ability to repair themselves from damage caused by loud noises or stress.
  • The repair process of these delicate cells involves a protein called XIRP2, which senses damage to the cores of the hair-like structures known as stereocilia, and then migrates to the damaged site to repair the cores by filling in new actin.
  • Understanding and enhancing the intrinsic repair mechanisms of hair cells could lead to the development of new treatments for hearing loss, including age-related hearing loss, and potentially impact associated conditions like Alzheimer's disease and other dementias.
  • How the cells that let us hear can repair themselves after being damaged

    School of Medicine researchers have discovered how the cells that let us hear can repair themselves after being damaged. That important insight could benefit efforts to develop new and better ways to treat and prevent hearing loss.


    “Hair cells” found in the inner ear, are important both for our ability to hear and our sense of balance. They are known as hair cells because the cells are covered in hair-like structures that serve as mechanical antennas for sound detection. When auditory hair cells are killed, as we learn in school, they are gone for good. But the new UVA Health research shows these delicate cells have the ability to repair themselves from damage caused by loud noises or other forms of stress.

    Want more breaking news?

    Subscribe to Technology Networks’ daily newsletter, delivering breaking science news straight to your inbox every day.

    Subscribe for FREE

    “For many years, auditory research has placed considerable emphasis on the regeneration of sensory hair cells. Although these efforts continue, it is equally important to enhance our comprehension of the intrinsic mechanisms that govern the repair and maintenance of these cells. By gaining a deeper understanding of these inherent repair processes, we can uncover strategies to fortify them effectively. One such approach in the future might involve the utilization of drugs that stimulate repair programs,” said researcher Jung-Bum Shin, PhD, of UVA’s Department of Neuroscience. “In essence, when replacement of hair cells proves challenging, the focus shifts towards repairing them instead. This dual strategy of regeneration and repair holds strong potential in advancing treatments for hearing loss and associated conditions.”

    HEARING REPAIR

    Hair cells are naturally fragile – they must be delicate so they can sense sound, but they also must withstand the continuous mechanical stress inherent in their jobs.


    Prolonged exposure to loud noise harms hair cells in a variety of ways, and one of those is by damaging the cores of the “hairs” themselves. These hair-like structures are known as stereocilia, and Shin’s new research shows a process they use to repair themselves.


    The hair cells do this by deploying a protein called XIRP2, which has the ability to sense damage to the cores, which are made of a substance called actin. Shin and his team found that XIRP2 first senses damage, then migrates to the damage site and repairs the cores by filling in new actin.


    “We are especially excited to have identified a novel mechanism by which XIRP2 can sense damage-associated distortions of the actin backbone,” Shin said. “This is of relevance not only for hair cell research, but the broader cell biology discipline.”


    The pioneering work has netted Shin and his colleagues more than $2.3 million from the National Institutes of Health, grant R01DC021176, to fund additional research into how the cores are repaired. By understanding this, scientists will be better positioned to develop new ways to battle hearing loss – even the kind that comes from aging, the researchers say.


    “Age-related hearing loss affects at least a third of all older adults,” Shin said. “Understanding and harnessing internal mechanisms by which hair cells counteract wear and tear will be crucial in identifying ways to prevent age-related hearing loss. Furthermore, this knowledge holds potential implications for associated conditions such as Alzheimer's disease and other dementia conditions.” 


    Reference: Wagner EL, Im JS, Sala S, et al. Repair of noise-induced damage to stereocilia F-actin cores is facilitated by XIRP2 and its novel mechanosensor domain. eLife. 2023;12:e72681. doi: 10.7554/eLife.72681


    This article has been republished from the following materials. Article summaries may be generated using fact-checked AI models. Note: material may have been edited for length and content. For further information, please contact the cited source.