Abstract
Many studies have been performed to clarify the underlying mechanisms of the release of ATP as an autocrine / paracrine signaling molecule. So far, there is a variety of findings on the mode of release of this nucleotide. This review focused on the possible mechanisms of ATP release. The ATP binding cassette, especially CFTR (cystic fibrosis transmembrane conductance regulator), is a strong candidate for a channel or a transporter for outward movement of ATP. CFTR, which is activated via phosphorylation by protein kinase A, causes an opening of channels for Cl− and ATP4−, releasing ATP. However, the possible involvement of CFTR in ATP release is still under dispute. As another candidate of the membrane machinery, the hemichannel of gap junction has been raised. Mechanical stress and photoliberation of caged InsP3 induce the release of ATP as a paracrine through the hemichannel accompanied with the increase of [Ca2+]i. These events result in the Ca2+wave as cell-to-cell communications. In conclusion, an authoritative view of the mechanism of ATP release remains to be made clear in future studies.
