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Keratinocytes are the first cells that come into direct contact with external tactile stimuli; however, their role in touch transduction  in vivo  is not clear. The ion channel Transient Receptor Potential Ankyrin 1 (TRPA1) is essential for some mechanically-gated currents in sensory neurons, amplifies mechanical responses after inflammation, and has been reported to be expressed in human and mouse skin. Other reports have not detected  Trpa1  mRNA transcripts in human or mouse epidermis. Therefore, we set out to determine whether selective deletion of  Trpa1  from keratinocytes would impact mechanosensation. We generated  K14Cre-Trpa1  fl/fl  mice lacking TRPA1 in K14-expressing cells, including keratinocytes. Surprisingly,  Trpa1  transcripts were very poorly detected in epidermis of these mice or in controls, and detection was minimal enough to preclude observation of  Trpa1  mRNA knockdown in the  K14Cre-Trpa1  fl/fl  mice. Unexpectedly, these  K14Cre-Trpa1  fl/fl  mice nonetheless exhibited a pronounced deficit in mechanosensitivity at the behavioral and primary afferent levels, and decreased mechanically-evoked ATP release from skin. Overall, while these data suggest that the intended targeted deletion of  Trpa1  from keratin 14-expressing cells of the epidermis induces functional deficits in mechanotransduction and ATP release, these deficits are in fact likely due to factors  other  than reduction of  Trpa1  expression in adult mouse keratinocytes because they express very little, if any,  Trpa1 .

Mechanosensory and ATP Release Deficits following Keratin14-Cre-Mediated TRPA1 Deletion Despite Absence of TRPA1 in Murine Keratinocytes