title: The C. elegans mitochondrial K+(ATP) channel: a potential target for preconditioning.
abstract: Ischemic preconditioning (IPC) is an evolutionarily conserved endogenous mechanism whereby short periods of non-lethal exposure to hypoxia alleviate damage caused by subsequent ischemia reperfusion (IR). Pharmacologic targeting has suggested that the mitochondrial ATP-sensitive potassium channel (mK(ATP)) is central to IPC signaling, despite its lack of molecular identity. Here, we report that isolated Caenorhabditis elegans mitochondria have a K(ATP) channel with the same physiologic and pharmacologic characteristics as the vertebrate channel. Since C. elegans also exhibit IPC, our observations provide a framework to study the role of mK(ATP) in IR injury in a genetic model organism.
authors.affiliation: Department of Pharmacology & Physiology, Box 604, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA.
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Wojtovich
authors.forename: Lindsay S
authors.initials: LS
authors.lastname: Burwell
authors.forename: Teresa A
authors.initials: TA
authors.lastname: Sherman
authors.forename: Keith W
authors.initials: KW
authors.lastname: Nehrke
authors.forename: Paul S
authors.initials: PS
authors.lastname: Brookes
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism*; D019194:Ischemic Preconditioning; D008928:Mitochondria / Q000378:metabolism*; D023421:Models, Animal; D015221:Potassium Channels / Q000819:agonists / Q000187:drug effects / Q000378:metabolism*; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D029742:Caenorhabditis elegans Proteins; D015221:Potassium Channels; C117780:mitochondrial K(ATP) channel