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Researchers at the National Institute for Physiological Sciences (NIPS) have reported that the transient receptor potential vanilloid 4 (TRPV4) ion channel in keratinocytes is important to maintain skin barrier function and prevent skin dehydation. According to these researchers, chemicals that modulate TRPV4 activity, could affect barrier repair of damaged skin.
The research, led by Takaaki Sokabe and Makoto Tominaga, was published in a report in the Journal of Biological Chemistry. According to the research, TRPV4 is a physiological sensor for hypo-osmorality, mechanical deformation and warm temperature.
The channel activation leads to various cellular effects involving Ca2+ dynamics. The researchers found that TRPV4 interacts with β-catenin, a component linking adherens-junctions and the actin cytoskeleton, thereby enhancing cell-cell junction development and formation of the tight barrier between skin keratinocytes.
A study conducted on mice, showed that a deficiency of TRPV4 resulted in impairment of the intercellular junction-dependent barrier function in the skin. The researchers reported, "In TRPV4-deficient keratinocytes, extracellular Ca2+-induced actin rearrangement and stratification were delayed, following significant reduction in cytosolic Ca2+ increase and small GTPase Rho activation. TRPV4 protein located where the cell-cell junctions are formed and the channel-deficiency caused abnormal cell-cell junction structures, resulting in higher intercellular permeability in vitro."
The researchers concluded that TRPV4 uses skin temperature to provide Ca2+ for cell-cell junction complexes to reinforce their tightness. Perhaps this research can be used to develop a raw material that maintains the skin barrier regardless of skin temperature.