While many of us wish we could regrow hair lost as we age, there are other hairs we might forget about – namely, the tiny ones in our ears that help us hear. Once we lose the sensory hair cells in the cochlea, they're gone for good, but now researchers have found a way to regrow them in mice, potentially paving the way for more effective hearing loss treatments in humans.
We start life with about 15,000 of those hair cells in each ear, but over time they die off due to exposure to loud noises, disease, infection and other natural causes. To add insult to (literal) injury, mammals are the only vertebrates that can't regenerate them, so any damage done is permanent.
But can we learn to take advantage of the techniques other animals use? Past research by the team behind the new study found that a group of receptors known as epidermal growth factor (EGF) help to stimulate new sensory hair cells to grow. This signaling pathway is present in mammals, but seems to be oddly silent.
"In mice, the cochlea expresses EGF receptors throughout the animal's life, but they apparently never drive regeneration of hair cells," says Patricia White, lead author of the study. "Perhaps during mammalian evolution, there have been changes in the expression of intracellular regulators of EGF receptor family signaling. Those regulators could have altered the outcome of signaling, blocking regeneration. Our research is focused on finding a way to switch the pathway temporarily, in order to promote both regeneration of hair cells and their integration with nerve cells, both of which are critical for hearing."
The researchers focused on one particular member of the EGF family – a receptor known as ERBB2. They tested three different methods to trigger this receptor to get the EGF pathway to fire back up and help replenish the lost hair cells. In the first, a virus was used to target the receptors. In the next, the team genetically engineered mice to overexpress ERBB2 which was already activated. And finally, the third involved testing two drugs designed to stimulate stem cell activity in other parts of the body, which also activated ERBB2.
However the ERBB2 pathway was activated, the team found that doing so set off a cellular chain reaction. First cochlear support cells proliferated, which activated neighboring stem cells to turn into new sensory hair cells. These new cells also integrated with the nerve cells necessary to send sound signals to the brain.
"The process of repairing hearing is a complex problem and requires a series of cellular events," says White. "You have to regenerate sensory hair cells and these cells have to function properly and connect with the necessary network of neurons. This research demonstrates a signaling pathway that can be activated by different methods and could represent a new approach to cochlear regeneration and, ultimately, restoration of hearing."
The new research was published in the European Journal of Neuroscience.
Source: University of Rochester
