title: Role of K+ channels in L-6 myoblast migration.
abstract: Migration of myoblasts is an important component of the reparative response to muscle injury, and furthermore may be a key determinant of the success of myoblast transplantation for the treatment of genetic muscle diseases. The present study examined the hypothesis that K+ channels modulate myoblast migration. The migration of cultured L-6 myoblasts was assessed in vitro on confluent cultures with the razor wound method, in the absence and presence of the following agents: 3,4-diaminopyridine and tetraethylammonium (which block several types of K+ channels), apamin and charybdotoxin (which block Ca++-activated K+ channels), glibenclamide (which blocks ATP-sensitive K+ channels), and alpha-, beta-, gamma-, and delta-dendrotoxin (which block voltage-gated K+ channels). Migration was assessed with respect to number of migrated cells, average distance migrated, and total distance migrated. Overall, myoblast migration was stimulated in response to low concentrations of tetraethylammonium, apamin, glibenclamide, and alpha-, beta- and delta-dendrotoxin. With these agents, the number of migrated cells increased by 28-47%, the average distance migrated increased by 22-35%, and the total distance migrated increased by 60-85%. Conversely, migration was inhibited by high concentrations of 3,4-diaminopyridine, tetraethylammonium, and all dendrotoxins. These data indicate that in L-6 myoblasts migration is regulated by K+ channels, and that several types of K+ channels appear to participate in cell migration.
authors.affiliation: Department of Medicine (Pulmonary Division), Louis Stokes Cleveland VA Medical Center, Case Western Reserve University, 10701 East Boulevard, Cleveland OH 44106, USA. exv4@pocwru.edu
authors.forename: Erik
authors.initials: E
authors.lastname: van Lunteren
authors.forename: Christopher
authors.initials: C
authors.lastname: Sankey
authors.forename: Michelle
authors.initials: M
authors.lastname: Moyer
authors.forename: Rudolf M
authors.initials: RM
authors.lastname: Snajdar
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism*; D002465:Cell Movement / Q000187:drug effects / Q000502:physiology*; D002478:Cells, Cultured; D018482:Muscle, Skeletal / Q000254:growth & development* / Q000293:injuries* / Q000378:metabolism; D032446:Myoblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated / Q000187:drug effects / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D012038:Regeneration / Q000502:physiology*; D014945:Wound Healing / Q000187:drug effects / Q000502:physiology*
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; D024642:Potassium Channels, Voltage-Gated; D000255:Adenosine Triphosphate