In a groundbreaking discovery, U.S. scientists have revealed that the epithelial cells in human skin, long believed to be “mute,” communicate in response to injury through a slow, bioelectrical signal—dubbed the “silent scream.” This finding challenges previous assumptions about these cells, which were once thought to lack any form of bioelectrical communication, and could lead to advancements in medical technologies aimed at speeding up healing.
The discovery was made by researchers at the University of Massachusetts Amherst, including polymath Steve Granick and biomedical engineer Sun-Min Yu. They were investigating cellular communication in the epithelium, the tissue layer that lines skin and organs. Using an innovative system with around 60 electrodes on a chip, the team simulated a wound to track the bioelectrical responses of lab-grown human keratinocytes, the primary cells in the skin’s outer layer.
Granick describes the newly discovered signal as “a slow, persistent scream” that spreads across large distances at speeds of approximately 10 millimeters per second. Unlike the rapid communication of nerve cells, this signaling is much slower—about 1,000 times slower than neuronal impulses. The signals, which propagate for hundreds of micrometers from the wound site, may last for several hours, indicating a prolonged cellular response.
The mechanism behind this communication relies on ion channels, which are small pores in cell membranes that allow charged ions, particularly calcium, to pass through. Unlike neurons, which respond to changes in voltage or chemical stimuli, these epithelial ion channels are triggered by mechanical stress, such as pressure or stretching. This novel form of communication in epithelial cells shares similarities with the way plants communicate damage to other parts of their structure, such as when they react to being eaten by herbivores.
The researchers were particularly intrigued by the persistence and duration of the signals, which can last up to five hours in some cases, far longer than typical neuronal signals. Despite these differences, the voltage levels of the signals are similar to those observed in neurons, cycling through the same phases of communication.
While the exact nature of the signal remains uncertain, with initial tests suggesting the involvement of calcium ions, this discovery paves the way for new biomedical applications. Devices such as wearable sensors and electronic bandages could potentially harness this slow, persistent communication to accelerate the healing of wounds.
“This new understanding of how cells communicate during injury opens up new possibilities for biomedical devices that could improve recovery times,” said Yu. “It’s an exciting step forward in understanding how our bodies respond to harm at the cellular level.”
As researchers continue to investigate this phenomenon, the potential for innovative technologies in the field of medical treatment appears limitless.
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