title: [The mechanism of ATP release as an autocrine/paracrine molecule].
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 ATP(4-), 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 InsP(3) induce the release of ATP as a paracrine through the hemichannel accompanied with the increase of [Ca(2+)]i. These events result in the Ca(2+)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.
authors.affiliation: Department of Pharmacology, School of Medicine, Fukuoka University. katsurag@fukuoka-u.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Katsuragi
authors.forename: Keisuke
authors.initials: K
authors.lastname: Migita
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D019898:Autocrine Communication / Q000502:physiology*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000502:physiology; D006801:Humans; D066298:In Vitro Techniques; D019899:Paracrine Communication / Q000502:physiology*
chemical_list: C505032:CFTR protein, human; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D000255:Adenosine Triphosphate