Astringency is described as an oral tactile perception occurring during the consumption of tannin-rich foods. This sensation, mediated by the trigeminal nerves, participates negatively to the flavor of foods leading to the rejection of food with high astringency by the consumer. The exact molecular mechanism of its origin and the nature of the sensory receptors activated are still under debate. Up to recently, the main hypotheses involved changes in the lubrication properties of the oral cavity triggering the activation of mechanoreceptors. Recently, we have put a new hypothesis involving the mucin MUC1 forward as an explanation of the origin of astringency. MUC1 is a transmembrane mucin with two subunits linked by non-covalent interactions. It is expressed at the surface of oral epithelial cells impacting on the surface lubrication and the anchoring of the salivary proteins composing the mucosal pellicle (MP). MUC1 is also described as a sensor of the external cellular medium. Thus, we have proposed that MUC1 aggregation by astringent compounds disrupts its two subunits, inducing two different and sequential mechanisms: an intracellular signalling pathway leading to the release of neurotransmitter activating trigeminal free ending nerves and a disruption of the MP increasing the friction forces at the surface of the mucosa. To investigate this hypothesis, we have developed an innovating in vitro model of oral mucosa based on the transfection of the TR146 oral epithelial cell line with genes coding for different isoforms of MUC1, which differ by the length of the variable number of tandem repeat (VNTR) module and the cleavage of proprotein at the origin of the 2 subunits. Stable expression clones have been selected and their ability to anchor salivary proteins and form the mucosal pellicle has been compared to the one of a previous TR146 cell line transfected with a non-cleavable isoform of MUC1 that do not have a VNTR module.