Functional expression of the transient receptor potential channel TRPA1, a sensor for toxic lung inhalants, in pulmonary epithelial cells

摘要: The cation channel TRPA1 functions as a chemosensory protein and is directly activated by number of noxious inhalants. A pulmonary expression has been described in sensory nerve endings its stimulation leads to the acceleration inflammatory responses lung. Whereas function neuronal cells well defined, only few reports exist suggesting role epithelial cells. aim present study was therefore (1) evaluate cell lines, (2) characterize TRPA1-promoted signaling these cells, (3) extra-neuronal this lung tissue sections. Our results revealed that widely used alveolar type II line A549 expresses at mRNA level. Furthermore, stimulating with known activators (i.e., allyl isothiocyanate) led an increase intracellular calcium levels, which sensitive blocker ruthenium red. Investigating coupled downstream cascades it found activation elicited ERK1/2 whereas other MAP kinases were not affected. Finally, using markers immunohistochemical approaches, non-neuronal detected distal parts porcine epithelium, also examining human TRPA1-positive staining co-localized both underlining observed pattern. findings functional provide causal evidence for TRPA1-mediated control upon registration toxic inhalants vivo.