The impression of “hot” and “cold” is greatly influenced by sensory neurons. Thermosensitive TRP channels are a group of ion channels that they express. For example, the 2021 Nobel Prize in Physiology or Medicine was given for the discovery that TRPV1 (active above 43°C) and TRPM8 (activated below 29°C) deliver the “hot” and “cold” messages, respectively, to our brains.
TRPV3, which is activated by warm temperatures (32–39°C), is largely expressed in skin keratinocytes but is hardly ever seen in sensory neurons. There was a lot of debate over the idea that skin keratinocytes in addition to sensory neurons also perceive temperature. It is additionally not closed whether the response of TRPV3 in epidermal tissue can be sent to the brain and elicits temperature sensation.
In this study, the research group focused on TMEM79, a protein that is expressed in skin keratinocytes like TRPV3 however whose capability isn’t surely known, to explore the investigation of TRPV3. The research is published in the journal Nature Communications.
In the first place, the research group overexpressed TRPV3 and TMEM79 in HEK293T cells and analyzed the TRPV3-mediated current responses. They discovered that TRPV3-mediated currents were smaller in cells that expressed TRPV3 alone than in cells that expressed both TRPV3 and TMEM79 together. This result shows that TMEM79 lessens TRPV3-mediated currents.
Then, at that point, the research group made TMEM79-deficient mice, and inspected the temperature-dependent behaviors using Thermal Gradient Ring with a donut shape. In the 25°C room temperature condition, wild-type mice preferred a floor temperature gradient of approximately 30.4°C. While TMEM79-insufficient mice quickly moved to a warmer temperature of 34.4°C. This proposes that mouse temperature sensation is impacted by the progressions in TRPV3-mediated currents in the endless supply of TMEM79.TRPV3-mediated currents were without a doubt bigger in the skin keratinocytes lacking TMEM79 than in those of wild-type mice.
This shows that TRPV3-mediated currents were inhibited by TMEM79 in normal conditions and that TRPV3-mediated currents were expanded without TMEM79.
Last but not least, the research team looked into how TMEM79 and TRPV3 co-expression reduce TRPV3-mediated currents in skin keratinocytes. TRPV3 proteins which are typically expressed in the plasma membrane moved to cytosolic space upon co-expression of TMEM79. As such, a decrease of how much TRPV3 proteins on the plasma film diminished TRPV3-mediated currents.
Likewise, it was observed that TRPV3 proteins were conveyed to the lysosomes with TMEM79, followed by TRPV3 degradation, which is steady with the decrease in the total TRPV3 proteins in the cell upon co-expression of TMEM79. Moreover, the research group found that TRPV3 makes an actual complex with TMEM79 on the plasma membrane.
The group of researchers came to the conclusion that the amount of TRPV3 proteins in skin keratinocytes that bind to TMEM79 regulates temperature sensitivity. These outcomes shut down the long-standing debate in regards to the conceivable association of skin keratinocytes in temperature detection. This could prompt the improvement of a method for controlling our temperature sensation by directing the function of TRPV3 or TMEM79.
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