Abstract
On nociceptive neurons, one important mechanism to generate pain signals is the activation of P2X3 receptors, which are membrane proteins gated by extracellular ATP. In this work, we have studied the recovery of recombinant P2X3 receptor expression in human embryonic kidney (HEK) cells. Our data demonstrated that HEK cells were not permissive for stable P2X3 expression, since the significant time-dependent cell loss. In vivo treatment with P2X3 receptor antagonist limited the effect. The expression of a single P2X3 point mutant Y393A, also largely accelerated cell death. We suggest the requirements of a permissive intracellular molecular machinery for appropriate receptor expression. The present report suggests that despite HEK cells are often used as recombinant expression system for the study a variety of receptors function, they represent a limiting permissive environment for P2X3 receptors.