This study aims to determine the potential mechanism by which MCs may invade the IVD joint, investigate tryptase effects on matrix degradation and chemotactic/vascular markers, quantify and validate protein expression of PAR2 in NP, AF and CEP regions of the human IVD via immunohistochemistry and western blot and to determine the therapeutic potential of PAR2A in a bovine ex vivo translational model and in human in vitro model for proof of concept. Here, F2RL1 is linked to atrial fibrillation.