A Japanese research team lead by head researchers Dr. Takaaki Sokabe of The Japanese National Institute for Physiological Sciences (NIPS) and Prof. Makoto Tominaga have detected that the TRPV4 ion channel present in skin keratinocytes plays a key role in creating and maintaining a barrier function for preventing dehydration.
The Journal of Biological Chemistry has reported the research findings.
NIPS High Voltage Electron Microscope
TRPV4, one among the Ca2+-permeable channels known as ‘thermoTRPs’ that are sensitive to temperature changes , is expressed in the skin and functions like a warm sensor (>27°C) and helps to select the preferred environmental temperatures for mammals. Researchers focused on the TRPV4’s alternate function as the skin keratinocytes have been found to express TRPV3, another thermoTRP that works like a warm sensor.
TRPV4 interacts with b-catenin that is an adaptive protein between the E-cadherin and actin filaments in cell to cell junction complex. Genetic removal of TRPV5 from keratinocytes causes the Ca2+-induced cell to cell junction formation that is immature and delayed. This results in leaky junctions. The intercellular type of junction depending skin barrier in the mice with TRPV4 deficiency became weak depicting a leaky intercellular pathway in comparison to wild-type mice. These phenotypes were found to be TRPV4-specifc, though they were not TRPV3 dependent.
According to Sokabe TRPV4 is likely to use the skin temperature to offer Ca2+ to cell-cell junction complexes for reinforcing their tightness. For example, dried up skin in cold places or seasons could be caused by the TRPV4’s low activity. The low activity is in turn due to the low temperature of the skin. Barrier repair of the damaged skin could be made possible by developing chemicals that modulate the activity of TRPV4.